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micro module 4
infection disease and immunology
| Question | Answer |
|---|---|
| def of infection; infection can proceed to what; infection can result in what; what is latin for it | invasion/multiplication of pathogenic microorganisms into the body; damaged tissues; disease; to corrupt |
| disease: latin meaning; def; what is characterized by | living apart; loss of homeostasis in the body from various causes; clinical mainfestations |
| human indigenous flora: def; when do we get them; some of them can be what type of flora; | more the 10 trillion microbiota reside on body and they do not cause disease; w/in a few days and weeks after birth; transient; |
| human indigenous flora: def of symbiotic relationship; | organisms existing together; |
| human indigenous flora: symbiotic relationship- def mutualism; def of commensalism; | symbiotic relationship benefits both organisms; symbiotic relationship only beneficial to one organism; |
| types of infection: def of exogenous infection;how is an exogenous infection acquired; def of endogenous infection; how does the endogenous infection move; | this pathogen overcomes host's external defenses and enters sterile tissue; community based or nosocomial infection; this infenction is when normal microbiota gains acess to sterile tissue; from one placein body to another |
| types of infection: def of opportunistic infection; | this infection is a change in host's defenses whichs leads to infection this change in host's defense causes decrease microbiota and weakened immune system and commensal seizes the opportunity to invade |
| human normal flora: what type of flora is located on . . . skin; oral cavity and URT; conjunctiva; | staphylococcus sp., propionibacterium acnes, carynebacterium sp.; strep. sp., staph. sp., neisseria sp., corynebacterium sp., candida albicans; staph. sp., neisseria sp., corynebacterium sp., strept. sp; |
| human normal flora: what type of flora is located on . . . intestinal tract; vagina; urethra | bacteroides sp, clostirdium sp, enterobacter sp, klesiella sp, pseudomonas, candida albincans; staph. sp, lactobacillus sp, strept sp, corynebacteria sp, candida sp, vaginalis; staph sp, enterococcus sp, escherichia sp, strept sp |
| stages of disease: incubation period- starts with what; ends when | microbe entry and increasing #s of microbes; when CM appear |
| stages of disease: def of prodromal phase; def of acme period; def of period of decline; period of convalescence | mild CM and are nonspecific; acute stage with specific CMs; CMs subside, immune system is winning; body is returning to normal and tissue is repairing |
| types of disease: def of clinical disease; ex. of clinical disease; def of subclinical disease; ex of subclinical disease | specific CMs; rubeola; few obvious CMs; EBV infection during childhood produces flu like CMs instead of mononucleosis |
| methods of transmitting disease: examples of direct methods; examples of indirect methods; | person to person by hand or object, respiratory droplets, contact with animals; contaminated foods, injection of contaminated soid, contaminated water, contact with fomites, arthropod bites |
| reservoirs: def of vector; def of carriers; def of animal; def of soil and water | arthropod transmitting the disease agent; usually recovered from disease or has disease agent as part of their normla flora it sheds disease agent to others; show no signs of disease usually can transmit agent of disease; contaminated with diease agent |
| disease behavior: what are the 2 types; def of communicable; def of concommunicable; ex of communicable; def of noncommunicable | communicable and noncommunicable; trasmissable infectious and contagious; aquired directly from the environment not easily transmitted; gonnorrhea; clostridium spores from soiled object enters cut |
| disease occurance: endemic def; endemic ex; def of epidemic; ex of epidemic; pandemic def; pandemic ex | constantly present in a specific population; lyme disease in certain areas of US; a higher than normal incidence in a population over a relative short period of time (outbreak); chlamydias in US; and epidemic worldwide; AIDs and influenza |
| establishment of disease: portal of entry of exogenous pathogens: what is this determined by; where are the entry sites | by the opportunity and virulence factor; abrasions, cuts, wounds, mucous membranes |
| establishment of disease: dose level- def; low dose exposure over time may not lead to disease, but what else can happen; | # of organmisms that must enter for a specific disease varies by species; immunity with some species |
| establishment of disease: organism pepetration/invasiveness of tissues- why does this vary; ex of virulance factors | due to virulance factors; adhesions, enzymes, toxins |
| establishment of disease: organism exits- where om body | respiratory sectretions, blood, open wounds, urine, feces, and insect bite |
| organism virulance factors- virulance aka; genes that regulate these factors in bacteria do what; what is this cluster known as; | pathogenic; clust together; pathogenicity islands |
| organism virulance factors- adhesins: def; what are they specific too; bacterial ones keep organism where; name the kinds of adhesions; def of capsule; def of pili; def of flagella; | they bind to receptor cells; cell type specific; keep an organism at a site; capsules, pili, flagella, M protein, cell internalization, actin tails; adheres and avoids phagocytosis; attaches to tissues; move to site |
| organism virulance factors- adhesins- def M protein; def cell internalization; def actin tails; | targets host cell receptor sites; causes phagocytosis in nonphagocytic cells to gain entrance; host cell actin allows movement of organism in host cell and from cell to cell |
| organism virulance factors- bacterial enzymes- def coagulase; ex of organism that has coagulase; def of streptokinase; ex. of organism that has streptokinase | forms fibrin clot in host and protects organism from phagoctic cells; staph. aureus; dissolves fibrin clots in host and allows the spread of organism to other sites; strept. sp. |
| organism virulance factors- bacterial enzymes- def of hyoluronidase; ex of organism that has hyaluronidase; def leukocidin; ex of organism that has leukocidin; | digests hyaluronic acid and allows tissue penetration; staph. sp and strept sp; destroys neutrophils and macrophages; staph sp., strept sp, certain bacilli; |
| organism virulance factors- bacterial enzymes: def of hemolysin; ex of organism that has hemolysin; | dissolve host blood cells which release iron from bacterial metabolism; staph sp, strept sp, clostridum sp |
| organism virulance factors- bacterial toxins- exotoxins: what gram stain; where located in bacteria; what is it made of; do antibodies respond to this; does it stimulate abs; what happens when toxin is released into the environment | + &-; cytoplasm; protein; yes; possible; affects different target tissues neurotoxins and enterotoxins; |
| organism virulance factors- bacterial toxins- endotoxins: what gram stain; where located in bacteria; what is it made of; do antibodies respond to this; does it stimulate abs; what happens when toxin is released into the environment | gram -; cell membrance located in cell wall; lipid polysaccharide peptide; no; non; cell disintergration where cell wall breaks down lipid A released and it causes endotoxin shock |
| organism virulance factors- bacterial toxins- exotoxins: give example; protein based means what; the anti toxin neutralizes the what; one pint of neurotoxin will destroy what | that an anti toxin can be produced against it; neurotoxin; the worlds population |
| toxoid conversion: exotoxins are what; proteins can be modified in the lab to do what; give example; | proteins; called toxoid conversion it is invactivated after converted and is given as an immunization to stimulate antibody production against it; toxoid made against clostridium tetani that causes tetanus, we receive this when we are immunized |
| lipid A gram - bacteria: when gram - bacteria are involved in septicemia there is a high risk for what; gram - bacteria die and release what; antimicrobial tx can result in what; results of lipid A | endotoxin shock; lipid a which is a component of outer layer outermembrance cell wall; large # of bacterial cells dying; circulatory collapse which acts as a vasodilator and this decreases the BP causes ischemia and hypoxia thus cell death |
| def of resident flora | consists of a huge and vaired population of microbes that reside permanently on all surfaces of the body |
| def of true pathogens | these are able to cause disease in a normal healthy host with intact immune defenses |
| def of toxigenicity | the microbes capacity to cause disease |
| def of zoonosis | diseases that can be transmitted to humans but are normally found on the animal population |
| def of toxemias | the is toxinoses in which the toxin is spread by the blood from the site of infection - ex tetanus |
| def of necrosis | cell and tissue death from accumulated damage |
| def of intoxication | toxinosis from ingestion of toxins |
| def of mixed infection; def primary infection; def secondary infection | several microbes astablish themselves simultaneously; first infection; infection after the first one |
| what is an infection that the host does not manifest disease | asymptomatic or subclincal |
| def septicemia | microbes are multiplying in the blood and present in large numbers |
| def of bacteremia or viremia | small numbers of bacteria or viruses found in blood, they are not necessarily multiplying |
| def of prevalence | the total number of existing coses with respect to the entire population |
| the cells and tissues designed to protect the body are collectively referred to as ___ | the immune system |
| healthy functioning immune system is responsible for what 3 things | surveillance of the body, recognition of foreign material, destruction of entities deemed to be foreign |
| Innate immunity is aka | non specific immuntiy |
| how many lines of defense is there, what kind of defense does the 1st two lines provide | 3; nonspecific protection against anything foreign in the body; |
| innate immunity: first line of defense: def ; examples; | any barriers that block invasion at the portal of entry, nonspecific; skin |
| innate immunity: second line of defense: def; examples | internalized system of protective cells and fluids; inflammation and phagpcytosis |
| what is responsible for most functions of the immune system (hint it is a cell) | WBCs |
| lymphoid organs (spleen, lymph noids and thymus gland) are involved in what | the defense mechanism |
| why are cells in in the immune system able to travel freely throughout all parts of the body | b/c of the relationship between the blood, lympn system etc. |
| innate immunity: 3rd line of defense: def, | adaptive and acquired on an individual basis as each foreign substance is encountered by WBcs lymphocytes (specific immunity) |
| reticulo endothelial system: def | a meshwork of CT that connects the cells and organs of the body together |
| communication between the immune system cells are controlled by what; | chemicals called cytokines; |
| cells: erythrocytes: where in body; function and lifespan | develop in bone marrow, no nucleus, circulate to transport blood and O2 to tissues;120 days |
| cells: dendtritic cells: where in body; function and lifespan | relative of macrophages throughout body; processing foreign matter and presenting it to lymphocytes |
| cells: mast cells : where in body; function and lifespan | tissue ;cells similar to basophiles the trigger inflammatory response/ allergic reaction; lifespan not determined |
| cells: neutrophils: where in body; function and lifespan | blood and tissues phagocytosis; active engulfers and likkers of bacteria; 2days |
| cells: basophils: where in body; function and lifespan; why are they similar to mast cells | tissues; inflammatory events and allergies; lifespan not determined; b/c they have a common origin |
| cells: eosinophils: where in body; function and lifespan | throughout body; active in worm and fungal infections, allergy and inflammatory reactions; 6 days |
| cells: lymphocytes: where in body; function and lifespan | mature in bone marrow and thymus; primary cells involved in specific immine reactions to foreign matter; |
| cells: monocytes: where in body; function and lifespan; when does its name change to macrophages | blood and then elsewhere; phagocytosis and then differentiate into macrophages and dendritic cells; when it travels in the tissue |
| what WBCs and granulocytes; what WBCs and Agranulocytes | neutraphils, eosinophils, basophils; lymphocytes, monocytes |
| lymphatic system: this transports lymph to where; once the interstitial fluid enters a lymphatic capillary it is called what; transports fats to blood from where; protects the body using what | away from the interstitial spaces to blood; lymph; digestive lacteal; lymphocytes and macrophages; |
| lymphatic cells: all lymphatic cells are produced where; | in the bone marrow |
| lymphatic cells: T lymphocytes- aka ; involved in ____ immunity; where do they mature; high concentration where; hormone thymosin helps do what; | T cells; cell and antibody mediated immunity; the tymus gland; in circulating blood; mature lymphocytes/ activate them |
| lymphatic cells: B lymphocytes- involved in ___ immunity; activated B cells produced what to destroy an antigen; antibody mediated immunity is aka; activated B cell will convert to what | antibody; antibodies; humoral immunity; a plasma cell |
| lymphatic cells: magrophages- these are monocytes lcoated where; primary function | tissue; phagocytosis, antigen processing, activating lymphocytes; |
| lymph nodes: name the locations; def; function | thoracic cavity, axillary nodes, inguinal, cervical, supratrochlear (medial arm), abdominal, pelvic; pea sized groups of nodes containing T cells, B cells and macrophages; filters lymph and macrophages protect; |
| what are the 4 major subdivision of the immune system | reticuloendothelial system, extracellular fluid, blood, lymphatic system |
| thymus gland: location; decreases in ___ as we age; what migrates here from Red bone marrow to mature; function; def of thymosin; | superior to heart; size; T cells; secretion of thymosin; hormone involded in T cell maturation |
| other lymphatic organs: spleen def; tonsils def; | filter blood filled with T cells, B cells and macrophages and blood pools there; small clusters of lymph tissue; |
| GALT: aka; what does it include; def; def of peyers patches; | gut-associated lymphoid tissure; peyers patches, appendix, lacteals; best developed lymphoid tissue; lymph tissue that line insestinal tract; |
| reticuloendothelial system: def; | network of connective tissue fibers the interconnect cells and provides a passageway for immune cells |
| what type of immunity is general no matter what type of pathogen is in play in the body | innate immuntiy |
| immune response: aka; host defenses divided into what two categories; innate immunity has what lines of defense; acquired has what line of defense | host defenses; innate nonspecific and acquired/ specific immunity; 1 nad 2; 3 |
| immune response: 1st line of defense- ex; def | physical barriers, chemical barriers, genetic components; a surface protection composed of anatomical and physiological barriers that keep microbes from penetrating the sterile body compartments |
| immune response: 2nd line of defense- ex; def; | inflammatory response, interferons, phagocytosis, complement; cellular and chemical system that comes into play when infectious agent makes it past surface defenses; |
| immune response: 3rd line of defense- what are the 2 kinds; what are the 2 kinds of naturally acquired; what are the 2 kinds of artificially acquired | naturally and artificially acquired; active and passive; active and passive |
| immune response: 3rd line of defense- ex of active naturally acquried; ex of passive naturally acquried; ex aof active artificially acquried; ex of passive artificially acquired | infection; maternal antibodies; vacciniation; immune serum |
| immune response: 3rd line of defense- these immunities create what; def of 3rd line of defense | antibodies, B cell, t cell and cytokinesl they must be developed uniquely for each microbe through the action of specialized white blood cells, this form of immunity is usually long term and has memory |
| immune response: 3rd line of defense: poli is ex of __ immunity; Rh-neg. pregnant mom give Rhogam is example of __immunity; intact skin is example of __ immunity; mono infection in teen is ___ immunity; moms antibodies from breast milk __ immunity | active artificially; passive artificially acquired; first line defense; active naturally acquired; passive naturally acquired |
| immune response: if it is active person has long or short term protection; if it is passive person has long or short term protection | long; short |
| non-specific innate immunity: this immunity is produced by what; is this present at birth; can it vary by race | general defenses to protect against many different kinds of organisms rather than a specific one or two; yes; yes; |
| non-specific innate immunity: first line- ex of physical barriers; ex. of chemical barriers; ex of genetic components; | skin and skin secretions; antimicrobial substances in body fluids, saliva, mucus, tears and saliva, gastric secretions; variations in host species |
| non-specific innate immunity: second line- ex; ex of molecular defenses | cellular defenses, infalmmation, fever, malecular defences; interferons and complement |
| 1st line: physical/chemical barriers-skin: b/c there are layers of dead cells that slough off that sheds what; what are skin secretions | organisms; sevum and sweat |
| 1st line: physical/chemical barriers-mucous membranes: it traps what; ciliated cells move mucus to __ and then it is what | microbes; pharynx and then it is swallowed |
| 1st line: physical/chemical barriers- acidity of stomach; what is pH; why decrease in microbes | 2; gastric juices kills most bacteria |
| 1st line: physical/chemical barriers- vagina- what is pH; the pH does what | acidic; releases some flora |
| 1st line: physical/chemical barriers- semen- what does it have | antimicrobial chemicals |
| 1st line: physical/chemical barriers- urine- urine flow does what | flow pushes out microbes |
| 1st line: physical/chemical barriers- bile and intestinal enzymes- function | helps detroy microbes |
| 1st line: physical/chemical barriers- lysozyme- ex; function | tears, sweat and saliva; destroys the cell wall of gram pos. bacteria |
| 2nd line- cellular/chemical response- interferons- what are the 3 types; they stimulate non-infectious cells to produce what; they are produced when; they inhibit the expression of what; | alpha, beta, gamma; antiviral proteins that block viral replication; when cells are virally attacked; cancer genes and has tumor suppressor effect |
| 2nd line- cellular/chemical response- phagocytosis- what cells are involved; | neutrophils, monocytes, macrophages; chemicals released by damaged host cells, pathogen associated malecular patterns |
| pathogen associated moleculat patterns: abrev.; includes what; | PAMPS; peptidoglycan, lipopolysaccharide of surface of pathogen |
| antiviral proteins block ___ replication | viral |
| what is used in the Tx of cancers | interferon |
| process of phagocytosis: def of phagocytosis; how many steps ; they cell is attracted to the bacterial cells by what; the cells; what is a phagosome; | cell eater; 5; the chemotactic factors; the foreign particles that are now in the phagocytic cell |
| process of phagocytosis: cells recognize some organisms as foreign b/c of the what; once the phagosome is formed what migrates to the scene; what do lysosomes do; once the bacterial is broken down what happens; | PAMPS; lysosomes; they use chemicals to break the bacterial cells apart; the debri is released |
| opsonization: aka; if the pathogen is coated with anitbodies of complement what happens; this binding provides what phagocyte what; | enhanced phagocytosis; these 2 structed bind to the phagocyte; a firm connection to draw in the bacteria; |
| inflammation- nonspecific defense: is it acute or chronic; ex of acute; ex of chronic; | both; cute in skin; damage to lining of Bvs; |
| inflammation: (acute)- cells damged release chemicals that signal what; example of chemical; chemicals cause what to happens; s/s of vasodilation and increased capillary oermeability | neutrophils and macrophages; histamine; vasodilation, and increased capillary permeability; edema, phagocytes to injured ares |
| inflammation: (acute)- why does vasodilation occur; what is next step after inflamation; what is step after phagocytosis; | so lymphocytes can go to area; phagocytosis; blood clot of affected area |
| inflammation: (acute)- the inflammatory response is a reaction to what; why does redness occur; why does warmth occur; | any traumatic event in the tissues; increased circulation and vasodilation to tissues; the heat given off by the increased flow of blood |
| inflammation: (acute)- the vascular changes are controlled by what; | cytokines released by blood cells, tissues and platelets in injured area; |
| inflammation: (acute)-what are the 4 chemical mediators that have vasoactive efffects; | histamine, serotonin, bradykinin, prostaglandins; |
| inflammation: (acute)- what is pus; what is a fibrin clot for ; s/s of inflamation; why won't tissue be as it was from before injury; | WBCs and debris generated by phogocytosis; the bodies attempt to protect the body; erythema, heat, edema, pain, and altered function; b/c of scar tissue |
| inflammation: chronic- why is it bad; | b/c it can harm our normal cells b/c of the enzymes released; |
| nonspecific defense- fever- what is name of substance that can increase our body temp; what produces pyrogens; pyrogens stimulate what part of the brain to incrase body temp; | pyrogens; by activated macrophages, bacteria, viruses and other microbes; the hypothalamus |
| nonspecific defense- fever- why is elevated body temp good; fever decreases blood iron why is this helpful in an infection; | bc/ increased phagocytosis and increased tissue repair in body; some organisms need iron and this will inhibit their growth |
| nonspecific defense- fever- why is the hypothalamus set point altered; why are high fevers bad | b/c a higher body temp is better for the immune response; b/c it is dangerous to the body |
| nonspecific defese- natural killer cell- this is a __ lymphocyte; what do they do; what protein is the abnormal cell lacking; | defensive; they survey tissue cells in body and they are looking for ones that lack the proper proteins on their surface (IE tumor cell, virally infected cells) and then they kill those cells; I MHC proteins; |
| nonspecific defese- natural killer cell- how does the NK cell kill abnormal cell; the eprforins and granzymes bore holes where; | after binding it inserts pore forming proteins called perforins and granzymes; in cell wall and kill the cell |
| nonspec. defense- complement system: how many blood proteins does it consist of; this is used to help destroy what; | 26; bacteria and viruses; |
| nonspec. defense- complement system: C3 activation- what are the 2 ways this pathway is activated; when C3 is activated this causes what; what is outcome of activation of the system; how does membrane attack kill the cell; | by binding to pathogen surface or antigen antibody complex; the activation of other complement proteins; inflammation, attraction of neutrophils, opsonization, membrane attack complexes that lyse the pathgoen; it burrows a hole in the cell and kills it. |
| def of opsonization | increased phagocytosis |
| what defenses are inborn | 1st and 2nd |
| what does whole blood consist of | blood cells disperseed in plasma |
| specific immunity: what line of defense is this; is it innate; is it adaptive; how is this immunity acquired; what are the two types of this; | the 3rd line of defense; no; yes; only after an immunization event; cell mediated immuntiy and antibody mediated immunity |
| antibody mediated immunity is referred to as what; | humoral immunity |
| def of immunocompetence; immunocopetence is distinguished by; | the ability of the body to react with muriad foreign substances; development of B and T lymphocytes, the lymphocytes become specialized for reacting only to one specific antigen or immunogen; |
| antigens: def; | molecules that stimulate a response by T and B cells that are proteins of polysaccarides on or inside cells and virusesl |
| specific immunity: what are the 2 characteristics of this line of defense; why is memory important; | specificity and memory; this can help with the rapid mobilization of lymphocytes that have been programmed; |
| activation of lymphocytes and clonal expansion: when antigens are present what happens; what are the 2 types of lymphocytes; since the B and T cells proliferate what does this create; these clones will only react to what; some of clones will be what | B and T cells proliferate and differentiate in response to the B and T cells; B and T cells; a clone or group of genetically identical cells; antigenic determinate; memory cells |
| clonal selection theory and lymphocyte development: def; these genetic changes generate what; b/c of the many diff. types and B and T cells each one recognizes diff what | early undifferentiated lymphocytes in the embryo,fetus, and adult bone marrow undergo a continuous series of divisions and gentic changes; different B and T cells in the body; antigenic determinates |
| clonal selection theory and lymphocyte development: all T and B cells are produced where; B cells mature where; when B cells are released where do they wait; where do T cells mature; when T and B cells reach the lymphoid system they are ready for what; | bone marrow; bone marrow; in the lymphoid system; the thymus gland; to respond to a unique antigen |
| preventing reactions to self: def clonal deletion; what disease are thought to be the cause by the loss of immune tolerance to self; when are the defective ones destroyed; | if a cell reacts to self they are destroyed during development through this process; autoimmune disease ; during fetal development are early childhood |
| def of immune tolerance | tolerance to self |
| activation of the immune response begins when | when a pathogen enters the body |
| the immune response: antigen presenting cells def; antigen presenting macrophage then interacts with what; | macrophages with antigen fragments displayed on their cell surfaces; a T cell that is stimulated by the antigen |
| origin of B and T cells: lymphocytic cells differentiate to what two cells ; cells destined to become B cells stay where; T cells migrate to where; after B and T cells mature where do they migrate to; | B and T cells; in bone marrow; the thymus; secondary lymphoid tissue; |
| def of antigen | a substance that elicits an immune response |
| antigen: it contains what; antigenic determinant is aka; def of antigenic determinant; abrev for antigens; aka; | antigenic determinant; epitope; portion of the antigen that the immune response id directed against; Ag; immunogen (Ig) |
| Hapten: is this a protein molecule; haptens binds to what; when is it recognized as an antigen; give ex | usually no; a protein first and the is recognized as an antigen; after it binds to the protein; penicillin, molecules in poisin ivy and cosmetics |
| immune response: is it controlled; why should it be controlled | yes; so it does not damage tissues in the body |
| examples of epitotes in bacteria | pilus, cell wall and flagella (Bc these all have protein in them) |
| host cell Proteins: def; what is MHC complex; | these are proteins found on host cell (our own cell); these are glycoprotein molecules that are immebedded in cell membrane and they are different from person to person, they can act as antigens (ex my RBC given to someone else) |
| MHC complex: aka; where is this found in cell; what kind of properties does it have; transplanted cells must express similar MHC complexes to decrease what; what people have same MHC | major histocompatibility complex; the cell membrane; antigenic; rejection of the cells or organs; identical twins |
| MHC complex: how many classes are there; what are the names of the 3 classes; class I found where; where is class I not found | 3; class I, II, III MHC proteins; all nucleated cells; erythrocytes |
| MHC complex: class II found where; class III proteins are found where; class 3 is found where; | only on B cells, macrophages and dentritic cells; all cells on body; complement; |
| MHC complex: ex- antgen enters lymphatic or CV system: what phagocytizes it process it and present it; what is the macrophage now referred to | macs or dendritic cells; antigen presenting cell; |
| MHC complex: what two cells can respond to antigen presenting cells; B and T cells can then activate what 2 things; | T and B cells in lymphoid tissue; cell mediated immunity, antibody mediated immunity aka humoral immunity |
| cell mediated immunity: T cells are activated against cells that display what; ex of cells that T cells are activated against in this immunity; what T cells are involved | unknown antigens or lack certain MHC-I proteins; virally infected cells; certain bacteria, tumor cells, transplanted tissue; helper T cells (CD 4+) and cytotoxic T cells (CD 8+) |
| cytoxic t cells - have what receptor; has what coreceptor; is it granuolated; what immunity is it involved in | T cell receptor; CD8 coreceptor; yes; cell mediated immunity |
| helper T cell: what is receptor; what is coreceptor; is it granulolated; they play are role in what type of immunity | T cell receptor; CD4 coreceptor; no; humoral and cell mediated immunity |
| cytokines/lymphokines: def of cytokines; def of lymphokines; wha can release cytokines; cytokines play a major role in what; | protein substances released by some of our cells; they affect other cells; lymphocytes produce various cytokines named these; dentritic cells macrophages etc; immune response |
| cytokines: macrophage chemotactic factor- where is it released; function | at or near antigen site; attracts macrophages to the antigen |
| cytokines:macrophage inhibition factor- function | keeps MACs from leaving the ag site |
| cytokines:macrophage activation factor- function; | makes MACs angry and it kills more efficiently, it increases macs function; |
| cytokines: tumor necrosis factor- function; | activates WBCs and cytotoxic to certain tumor cells |
| cytokines: interferon- function; what are the three types; | inhibit viral replication; alpha, beta,gamma |
| cytokines: interleukin- function; how many are there; are the the diff. types named | activate B cells, T cells and other immune cells; 18, IL 1-18 |
| cytokines: what two types are sometimes used to treat cancers; what kind enhances inflammation and helps in the with some auto immunity | IL-2 and interferon; tumor necrosis factor; |
| process of cell mediated immunity: what is the priamry response; what response has a long lag time of days or weeks; why is there | this is when you are first exposed to the antigen; primary response; b.c the cells are being activated so they can respond properly |
| process of cell mediated immunity:in the primary response with is a slow build up of what cells; what clones are produced; when is there an anamnestic response; why is there a shrot lag time in second response; in re-exposure, is T cell buildup slow or fa | activated T cells; memory T cells; re-exposure to Ag; b/c memory cells where produced in first infection; fast , b/c they are from memory cells |
| types of lymphocytes: T- helper cells- they start out as what; what activates them; what do naive cells divide/ mature into; | Naive Tcells and mature into effector cells; binding of an antigen presenting cell binding and interleukin when; effectos cells; |
| types of lymphocytes: T- helper cells- effector cells are aka; name the 3 effector cells; T helper 2 cells can help control immune response in what ways; | clones; memory T cells; T helper 1 cells, T helper 2 cells; activate humoral immunity and slow down T 1 cell response; |
| types of lymphocytes: cytotoxic T cells- aka; what activates them | T killer cells; dentritic, macrophages and cytokinees or by dividing into effector cytotoxic cells and memory cytotoxic cells |
| Cell mediated immunity: This immunity is the response of what cell; Before T cells are activated they must have ____ offered by what cmplex; T cells recognize an antigen only when what; | T cells; the antigen offered by the MHC complex; it is presented in association with an MHC carrier; |
| Cell mediated immunity: a macrophage has what 2 receptors on its surface; they antigen is ___ by the macrophage; once the macrophage phagocytises the antige what is it called; | MHC1 and MHCII; phagocytizes; antigen presenting cell ; |
| Cell mediated immunity: after phagocytized what happens to the antigen; antigenic component once processed by the MAC is moved to what; | it is broken up by MAC; the MHC2 receptor; |
| Cell mediated immunity: the antigen components that moved to the MHC2 receptor is called what; where does APC MAC move to after all of this; | the antigenic determinant or the epitote; lymphoid tissue |
| Cell mediated immunity: once in lymphoid tissue the MAC begins to circulate in the tissue until it can find ___ to bind to; what part of the naive T cell binds to the MHC2 receptor; what binds to the epitope; | a naive T cell; the CD4 coreceptor; the T cell receptor; |
| Cell mediated immunity: once the Tcell is bound to the MAC, what does the MAC secrete; what does IL1 stimulate; what happens nextl | (interleukin) IL 1; the T cell to undergo mitosis; naive t cell releases from mac and begins to divide |
| Cell mediated immunity: when t cell is dividing what is released from it; why does the t cell divide; what does IL 2 do; | interleukin 2; to produce an army of clones the recognizes that particular antigenic peptide; cause T cell to mature and differentiate; |
| Cell mediated immunity: what do the naive t cells differentiate into; what T cell activates B cells and humoral immunity; | memory T cell, t-helper 2 cells, T-helper one cells; T-helper 2 cells; |
| Cell mediated immunity: T helper one cells bind to what; why does Thelper 1 cell bind to macrophage; | infected macrophages; to stimulate its phagocytosis; |
| Cell mediated immunity: what kind of immunity is this | cell to cell combot |
| Cell mediated immunity: activation of cytotoxic Tcells- cytotoxic cells are stimulated by what; in this process the APC moves in lymphoid tissue until it finds what; | the MAC with the antigenic presenting component; the cytotxic cell t cell; |
| Cell mediated immunity: activation of cytotoxic Tcells- the cytotoxic T cell binds how; the cytotoxic T cells are matures how; | the CD 8 coreceptor binds to the MHC2 on the surface of the MAC: same as naive Tcells by interleukin 1 and 2 |
| Cell mediated immunity: activation of cytotoxic Tcells- after the cytotoxic cells mature what do they do; what happens after it binds to MHC1; | they move to all parts of the body looking for cells that are presenting the antigenic determinate on MHC1 receptor; granzymes and porferins are released and enter into the cell membrane of infected cell and it lyses' |
| anti-body immunity: aka; why is it called humoral immunity; how many responses are there;name the 2; | humoral immunity; ; b/c antibodies are produced are they circulate in the body fluid; 2; primary and anamnestic response |
| anti-body immunity: primary response- when does this happen; is the lag process fast or slow; is it slow or fast to protect; what is the first Ab class to protect; what is the second class to protect; what memory cells are produced against the Ag; why doe | in the first exposure to Ag; slow/long; slow; IgM; IgG; memory B cells |
| anti-body immunity: anamnestic response- when does this occur; when is the response; Ab response is stronger or weaker; what Ab is produced; | re-exposure to same Ag; w/in hours; stronger; only IgG |
| anti-body immunity: primary- why does IgM change to IgG; | b/c there is a chem. signal |
| anti-body immunity: everytime we are exposed to the antigen this is called what; a booster is helpful how; | a booster; it makes our immune response stronger then last exposure; |
| anti-body immunity: how many responses can there be; name the 2 responses; | 2; T-independant and T-dependent; |
| anti-body immunity:what is Ab produced 1st in first exposure; what is Ab produced in 2nd exposure; | IgM; IgG |
| anti-body immunity: T-dependant- what cells are exposed to the antigen; the antigen binds to what; how is Ag able to bind to the surface receptor on the B cell; | B cells; the surface receptors on the B cell; b/c the antigenic determinate of the activates the B cell; |
| anti-body immunity: T cell dependant- once the Ag is bound to the B cell what happens; where is it presented; | the B cell then pulls the antigen into itself where it is processed and then presented; MHC2 receptor |
| anti-body immunity: T cell dependant- what is being presented on the MHC2 receptor; as the activated B cell moves throughout the lymphoid tissue what will it come in contact with; | the peptide fragment of the antigen; an activate T helper 2 cell; |
| anti-body immunity: T-dependant- the T helper 2 cell will recognize and bind to what; what on TH2 cell will bind to peptide fragment; what on TH2 cell will bind to MHC2 receptor; | the peptide fragment on the B cell; the TC4 receptor; CD4 coreceptor; |
| anti-body immunity:t-dependant: the TH2 cell will release what to stimulate the Bcell; after separation from the TH2 cell what does B cell do; | IL 2,4, 5,6; it divided and makes clones |
| anti-body immunity: T-dependant- what 2 types of cells does the B cell divide into; what are memory B cells used for; plasma cells secrete what; | memory cells and plasma cells; a more rapid response on second exposure; antibodies |
| anti-body immunity:t- dependent- in first exposure what is first antibodie produced; what is antibody produced in second exposure; | IgM; IgG; |
| anti-body immunity: what type T-dependent or T-independent is strongest; | T-dependent; |
| do antibodies do the destroying; | no they just mark the cell so macrophages know it has to be destroyed |
| anti-body immunity: T-independent- when an antigen enters the body what is it looking for; once bound the B cell brings the antigen into the B cell processes it and then__-_; | a B cell that can bind with the antigenic determinant on the antigen; that is as far as it goes - - -it does not present it on its surface; |
| anti-body immunity:T- independant: after this what does B cell do; what cell does B cell divide into | it begins to divide; palsma cells only and then the cells secrete IgM and IgG |
| anti-body immunity:independent- why is it weaker; | b/c no memory cells are produced this is only ; |
| superantigens: def; what does this aAg bind to; this binding results in what; | a class of antigens that don't need to be processed by MAcs; directly to MHC 3 proteins and to T helpers cell; cross linking; |
| superantigens: cross linking causes what; what is an immune storm; with high numbers of T helper cells causes a hypersecretion of what; this hyper secretion does what to body; give examples | an immune storm; an abnormally high number of T helper cells activated and they become hyperactive; cytokine (interleukin etc); CV shock and death; |
| Antibodies: aka; what class of proteins is it; what are the type types; def of monospecific; def of bivalant; | immunoglobulins; globulins; monospecific and bivalent; bind to 1 specfic antigenic determinant; binds to 2 antigenic determinants; |
| antibodies: what type of binding does IgG have; how long do they last in circulation; can they enter cells; | bivalant; 4 -23; no; *** be able to diagram the structure |
| antibodies: structure- how many heavy chains; how many light chains; what region binds to aG; what is it linked by; what area can bind to Fc recetpors; | 2;2; the variable region; disulfide bonds; the Fc portion |
| antibodies: what are the 5 classes of them; | IgG, IgA, IgM, IgD, IgE; |
| antibodies: IgG: # of binding sites; % of total body serum; average half life; crosses placenta; fixes complement ;biological function | 2, 80%; 23; yes; yes; long term immunity, memory antibodies |
| antibodies: IgA: # of binding sites; % of total body serum; average half life; crosses placenta; fixes complement ;biological function | 4; 13%; 6; no; no; sectretes antibodies, located on mucous membranes |
| antibodies: IgM: # of binding sites; % of total body serum; average half life; crosses placenta; fixes complement ;biological function | 10; 6%; 5; no; yes; produced at first response to antigen, can serve as B-cell receptor |
| antibodies: IgD: # of binding sites; % of total body serum; average half life; crosses placenta; fixes complement ;biological function | 2; 1%; 3; no; No; receptor on B cell; |
| antibodies: IgE: # of binding sites; % of total body serum; average half life; crosses placenta; fixes complement ;biological function | 2; <1%; 2.5; no; no; antibody of allergy, worm infections Fc portion binds to basophils or mastcells, |
| monitoring antibody production over time: complement fixation: what type of antibody can activate compliment; by activating compliment this initiates what; compliment binds to what | IgG and IgM; the distruction of the antigen; the antibody which binds to the antigen |
| monitoring antibody production over time: opsonization: def; Fc porion of antibody binds to what; b/c of the binding the MAc can do what more easily | antibodies coat and bind to the antigenic determinant; the Fc receptor on a MAC; destroy the antigen |
| monitoring antibody production over time: neutralization: def; | if the antibody binds to the surface of a virus or bacterial exotoxin it then blocks it from having an effect in the body this beutralizes them until they leave our body |
| monitoring antibody production over time: agglutination: def; with agglutination the cells will be destroyed how | this aB binds to the antigenic determinant on the antigen and b/c teh cells are bivalant they will cross react and then the cells will bind to eachother agriganting it; they will leave the body |
| which antibodies can activate compliment | IgG and IgM |
| which antibody has increased binding sites and increases complement activation | IgM |
| IgM rubella antiboies were detected in a fetus during the 5th gestational month, what does this mean | IgM fetal antibdoeis can be produced after 5-6 mo and indication and intrauterine infection; IgM cannot cross the placenta |
| which antibody is present in external secretions | IgA |
| IgG rubella anitbodies were detected in a pregnant woman; what does this mean | not a current infection or has passed the infectious stage of the disease |
| vaccinations: what kind of immunity is this; def of a vaccination; what response does this stimulate; wwhat was first vaccine | active artificial immunity; exposing a person to material that is antigenic but not pathogenic a primary and secondary anamnestic response to prime the immune system for future exposure to a virulen tpathogen; smallpox |
| principles of a vaccination: it should have low levels of what; it should protect against what; it should stimulate what; | adverse side effects or toxicity and not cause seroius harm; against exposure to natural wild forms of pathogen; both antibody and cell mediated response; |
| principles of a vaccination: it should have long term what; it should not require numorous what; should it be expensive; | lasting effects- produce memory; doses and boosters; no it should be easy to administer and have long shelf life |
| constructing vaccines: what are they made of; what is atenuation; | killed or inactivated pathogens; this is a strain that loses its virulence but retaines many of its antigens and can still elicit an immune response; |
| constructing vaccines: def of recombinant vaccine; | cloning the genes for a structure of the pathogen into a host microbe (Heb B) |
| constructing vaccines: what are the 3 categories; | whole cell vacciens, rocombinent vaccines; vacciens from microbe parts |
| constructing vaccines: whole cell vaccines- what are the 2 types; def of attinuated; how does the the killed/inactivated one cause infection; pathogen present | whole cell is killed or inactivated virus and live attinuated cells; weakened virus; although it is not live body reacts and makes antibodies; yes-does not cuases disease |
| constructing vaccines: vaccines from microbial parts- def; is pathogen present | virus is broken down into parts and small part is given into an injection and body will produce antibies ; yes |
| constructing vaccines: recombinant vaccine: def; ex; is there a pathogen present; | these cells contain there own DNA and DNA from another source; HEp A; no, antigen stimulates the immuntiy |
| do macrophages appear first and begin pahgocytosis in inflammation | no |
| what type of moncyte has a long tine process to trap pathogens near the surface of the body | dendritic cells |
| what molecule acts to draw phagocytes to foreign substances | PAMPs |
| which type of WBC granules contain peroxides and are particularly attracted to sites of parasitic worms | eosinophils |
| what is the name for any substance that elicits an immune response | antigen |
| what is not a benifit of fever | the inhibition of cell mediated immunity |
| the granules of basophiles and mast cells contain what | histamine |
| what is the name for the circulating substance that affects the hypothalamus and initiates fever | pyrogens |
| The immunoglobulin class that has a dimer form found in mucus, saliva, colostrum and other body secretions is | IgA |
| The embryonic yolk sac, the liver and the bone marrow are sites where what occured | Stem cells give rise to immature lymphocytes |
| Which process involves a more rapid synthesis and greatly increased titer of antibody when the immune system is subsequently exposed to the same antigen? | Anamnestic response |
| An activated TH cell produces ___ which is a growth factor for T helper cells and cytotoxic T cells. | Interleukin-2 |
| _____ is the most abundant class of antibodies in serum. | IgG |
| Antigens that elicit allergic reactions are called | Allergens |
| The most significant cells in graft rejection are | Cytotoxic T cells |
| MHC molecules are found on each of the following cells except | Erythrocytes |
| During presentation of APC-bound antigen, macrophages and dendritic cells secrete the cytokine, _____, that activates T helper cells. | Interleukin 1 |
| Which lymphocytes lack specificity for antigen and are cells that attack cancer cells and virus-infected cells? | Natural killer (NK) cells |
| Small foreign molecules that are too small by themselves to elicit an immune response are termed | Hapten |
| Plasma cells secrete what | antibodies |
| The immunoglobulin class that has an Fc region that binds to receptors on basophils and mast cells is | IgE |
| The molecular fragment on an antigen molecule that a lymphocyte recognizes and responds to is called a/an | Epitope |
| Cytotoxic T cells (Tc secrete what | grnazymes and perforins that damage target cells |
| hypersensitivity: def; how many types; name the types | exaggerated or inappropriate immune response that causes damage to tissues; 4; immediate hypersesitivty, antibody mediated; immune complex; t cell mediated |
| hypersensitivity: what type involves B cells; what type involve T cells; | 1-3; 4; |
| Type one hypersesitivity: aka; examples; what happens in first expsure; | IgE mediated ; anaphylaxis, allergies like hay fever asthma; exposed to allergen and stimulates the immune system the allergen then will be taken up be antigen presenting cells (Bcells, MAC) |
| Type one hypersesitivity: after the allergen is taken up by the APC, what happens; | T hellper 2 cells further activate the B cells causing cell mediated immune responses and antibody mediated immunity (clones of be cells and plasma cells are produced; |
| Type one hypersesitivity: what antibodies are secreted after plasma cells are produced; the production of IgE is different how; IgM Ab stimulate what; | IgE antibodies; IgM are usually produced; the mast cells |
| Type one hypersesitivity: where are mast cells located; IgE binds to what on the mast cells; | in the linign of the digestive tract, Resp. tract; the Fc receptors; |
| Type one hypersesitivity: now that the IgE Ab is boudn to the Fc receptors what is this called; after 1st exposure what is result; | the persom is considered "sensitized to the allergen; sensitized mast cells line those areas of the body; |
| Type one hypersesitivity: is there an allergic response in 1st exposure; what happens with seconds exposure; what does allergen cross link with; this cross linkage causes what; | no; allergen enters bodu and cross links; IgE sensitives mast cells; degranulation; |
| Type one hypersesitivity: how does degranulation occur; ex of chem mediators; s/s of second exposure localized | chemical mediators are released; histamines, serotonin, leukotrienes; inflammation, smooth muscle contraction, increased mucus production |
| Type one hypersesitivity: what is name for localized allergic reaction; what is s/s of allergic reaction throughout body; | atopic; systemic- dialed Bv/, |
| systemic anaphylaxis: what is this induced by; do s. muscles contract or dilate; more or less mucus production;increaseed or decreased cap. permeability; what happens to airways; what happens to BP; | chemical mediators; contraction; more; increased; they constrict; drops; |
| systemic anaphylaxis: s/s of increased cap. permeability; why hypovolemia; why low BP; hypotension causes what; | edema; b/c fluid is interstitial; b/c hypvolemia; organ failure |
| Type one hypersesitivity: what substances can cause this reaction; why does the tissues under mucous membranes hold most of the IgE Ab; what stimulates the B-cells to differenciate into IgE producing plasma cells; w | dust, pollen, dander, penicillin; b/c they happen to be rich in supply with these; cytokines; |
| Type one hypersesitivity:what cell produces the chemicals that produce a hypersensitivity response; where in body are mast cells located in high concetration; | mast cells; lungs, skin, GI, GU; |
| charecteristics of mast cells: what do they bind to during sensitization; what is unique about their granules; they have a tendancy to release what when triggered by a allegen; what is this releasing called | IgE; the contain physiologically active cytokines; the content of their granules; degranulation |
| Control of type 1 hypersensitivity: what is common way; what is done; this increases what cdells; this decreases what cells; why will this decrease IgE; T suppresors decrease what; | desensitization; small doses of antigen is given over long time; T suppresor cells and IgG; IgE response to aG;b/c IgG will bind to the Ag preveting IgE binding; IgE production |
| Type 2 hypersensitivity: aka; def; this reaction leads to what; ex that cause this; | cytotoxic reactions; specific Ab react with cell surface antigens interpreted as foreign; phagocytosis, cytotoxic t cell activty, complement mediated lysis; mismatched blood given to a recipient, Rh+ infant Rh- mom; |
| Type 2 hypersensitivity: blood groups: blood type A has what antigen on erythrocyte; type A has what antibody; type B what Ag; type B what Ab; type AB what Ag; type Ab what Ab; type O what Ag; type O what Ab; what is universal donor; universal acceptor | A; anti-b; B; anti-A; A and B; none; none; anti-a and anti b; O; Ab; |
| Type 2 hypersensitivity: blood groups:why can AB receive anytype of blood; | b/c they lack any agglutination antibodies to react; |
| type 3 hypersensitivity reaction: aka; what does this result from; the offending agent is always what; s/s ; end result; ex | immune complex; antigen-antibody complexes continuously being formed; present and activating B cells and Antibodies continuously react to antigens; inflammation, increased phagocytosis, increased complement activation; tissue damage; RA, lupus autoimmune |
| type 3 hypersensitivity reaction: what 2 things are bound together; what causes tissue damage; | antigens and Abs; enzymes released by neutraphils |
| hypersensitivity reaction: what is origin for 1st 3; what reactions involve Abs; what is Ab for type 1; what is Ab for type 2 and 3; | B cells; 1-3; Ige; IgG and IgM; |
| type 3 hypersensitivity reaction: what type of immune complexes are easily removed, and what ones are not; what releases enzymes responsible for tissue damage | large ones, intermediate ones; neutraphiles |
| hypersensitivity reaction: what cells are involved in type one; type two; type 3 | mast cells basophils; RbC WBC and platelets; host tissue cells; |
| hypersensitivity reaction: chemical mediators- type one; type 2; type 3 | histamine, serotonin,leukotrience prstaglandins; compliment activation; complement activation |
| hypersensitivity reaction: compliment activation leads to what in type 2 and 3 | enhanced phagocytosis, inflamation, membrane complex attack molecules; |
| hypersensitivity reaction: how long does it take for s/s in type 1; type 2; type 3 | <30 min; 5-8 hours; 2-8 hours |
| hypersensitivity reaction: s/s in type one | rash, inflamation respiratory, nasal cavity, GI, systemic |
| Type 4 hypersensitivity: aka; when are s/s evedent; why does it take so long for s.s; | delayed hypersensitivity; >12 hours; b/c reactions are mediated by type one T helper cells, not antibodies |
| t helper one cells are sometimes referred to as thwat; | delayed hypersensitivity t cells |
| hypersensitivity reaction: what type is not medaited by Abs; what is this type medaited by; all other types are mediated by what | type 4; T helper 1 cells; Abs |
| Type 4 hypersensitivity: what happens in first exposure; what happens in second exposure; s/s of release of cytokines; examples | activation of T helper 1 cells and normal immune response; the t helper one cells that were previously activated will begin to release cytokines; inflammation, eczema, swelling, raised hardened area; contact dermatitis, TB, |
| contact dermatitis is caused from what | metals, ingrediant in beauty products; |
| Type 4 hypersensitivity: what cell presents that antigen on its surface to stimulate the t helper one cell; what produces the s/s | dentritic cell; macrophages release substances that show a strong local inflam. response |
| TB skin test: what does it use; what is the name of the test; what are s/s of negative; what are s/s of positve; | purified protein derivative of killed mycobacterium Tb; Manitoux test; no skin raction; vesicle, erythema and induration; |
| TB skin test: how long does it take to show that it is positive; positive indicates what; | 48-72 hours b/c it is a delayed hypersensitivity reaction; person is sensitized - active or past infection |
| autoimmune disorders: myastenia gravis= what blocks the ACh reaceptor preventing Ach binding at the neuromuscular junction; s/s of this; the aCh forms what; | autoantibodies; progressive muscle weakness; a junction in the skeletal muscle fiber preventing the fiber from being stimulated |
| autoimmune disorders: RA- def; what releases enzymes | destruction of cartilage in joints, other tissues also damaged by autoantibodies; neutrophils |
| immunodeficiency diseases: hyposensitivity of the immune system- def of primary diseases; def of secondary disease | present at birth, congential and stemming from genetic errors; acquired after birth and caused by natural or artificial agents; |
| immunodeficiency diseases: AIDS- what type is it; the HIV destroys what; this destruction interupts what immune response; | secondary; CD4+ cells - te helper cells; both cell mediated and antibody medaited immunity |
| transplants: how many types of grafts; def of autograft; def isograft; def allograft; def xenograft; autograft | 4; self graft; graft between genetically identical individuals; graft between members of the same species; graft between members of different species; autograft |
| graft rejection mechanisms: the immune system interprets the tissues as what; how many forms of rejection; | nonself b/c it has wrong MHC complex; two; |
| graft rejection mechanisms: form one: the cytotoxic te cells are stimulated by what; the cytotoxic selfs attack and destroy what; how do they destroy it; | activated T helper cells; tramsplanted cells; perforin; |
| graft rejection mechanisms: form two: T helper cells are stimulated by what; they then release what; what does lymphokines do; | the APC; lymphokines; phagocyte and secretes lysosomal enzymes and destroy tissue; |
| GRaft v.s host rejection: what happens; most common in what transplant; what has to be suppressed | transplanted cells form immune products against host cell antigens; bone marrow; host immune cells |
| antirejection mechanisms: goal is what; what drugs are used; what can suppress imflammation; | immunosuppresion; antimitotic drugs and antilymphocyte antibodies; steroids; |
| serologic tests: electrophoresis: what is applied to the agarose; why is electric current applied; used for what | Ag and Ab; this diffuses the molecules to each other at different rates; to ID unknown antigen or antibody |
| eLISA: the wall is bound with what; this antigen bound to wall reacts with what; when the tube is washed out what remains; whatis added next to tube; what is added after anti-AB; what will show reaction | antigen; the antibody being detected; bound antibody; anti-antibody enzymes and tube is washed out; substrate thatreacts with enzyme present; color |
| western blot test: what does it confirm; done after what; what is isolated from PT; the proteins are transferred to what; whatis added to the blot; reaction shoews what | virla antigens that pts Abs are against; pos. ELISA; HIV proteins; cellulose paper- blotting paper; pt serum; colored bands b/c ab react wi separated proteins |
| monoclonal Ab: ab is injected into a most and what is removed; the plasma cells are then fused with what; hybridoma cells produce pure what; these abs are used in what; | plasma cells; myelomacells to produce hybridoma cells; Abs; researche for vacines |
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