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exam 3 micro
innate immunity, adaptive immunity, immunization and testing, immune disorders
| Question | Answer |
|---|---|
| species resistance | resistance due to the cells and physiological processes of humans that are incompatible with those of most plant and animal pathogens |
| when are we confronted with pathogens | everyday |
| first line of defense | external physical barriers to pathogens (skin and mucous membranes) |
| second line of defense | internal and composed of protective cells, bloodborne chemicals, and processes that inactivate or kill invaders |
| third line of defense | responds against unique species or strains of pathogens |
| innate defenses | non-specific-->first line defenses, phagocytosis, inflammation, complement system |
| adaptive defenses | specific-->humoral immunity and cell-mediated immunity |
| body's first line of defense is | made up of structures, chemicals, and processes that work to prevent pathogens entering the body |
| what does the first line of defense include | skin and mucous membranes of respiratory, digestive, urinary, and reproductive systems |
| epidermis | multiple layers of tightly packed cells, shedding of dead skin cells removes attached microbes (dendritic cells) |
| dermis | contains protein fibers (collagen), give skin strength and pliability to resist abrasions that could introduce microbes |
| sweat glands | secrete perspiration which contains salt, demcidins, and lysozyme |
| dermicidins | broad-spectrum antimicrobial peptides found in eccrine sweat glands |
| sebum is secreted by | sebaceous (oil) glands |
| sebum | helps keep skin pliable and less likely to break or tear, contains fatty acids that lower the pH of the skin to about 5 |
| mucous membranes ar e a | less efficient barrier to the entrance of pathogens |
| mucous membranes protect with | thin, outer covering composed of tightly packed living cells, continual shedding and replacement of cells carries attached microorganisms away, dendritic cells phagocytize invaders and extend pseudopods bw epithelial cells to sample contents of the lumen |
| mucous membranes protect with 2 | sticky mucus that traps microbes, ciliated columnar cells whose cilia propel mucus and trapped particles, lysozyme and antimicrobial peptides found in mucus |
| lacrimal apparatus in innate immunity | group of structures that produce and drain away tears |
| tears | join the nasal mucus and flow into the pharynx, where they are swallowed (lysozyme) |
| blinking | spreads tears and washes the surfaces of the eye |
| normal microbiota | helps protect the body by competing with potential pathogens (microbial antagonism) |
| activities that normal microbiota make pathogens hard to compete | consumption of nutrients make them unavailable to pathogens, create an environment unfavorable to other microorganisms by changing pH, attach to all sites on human cells making it difficult for pathogen to attach |
| activities that normal microbiota make pathogens hard to compete 2 | help stimulate the body's second line of defense, can produce antimicrobial compounds for defensive purposes, promote overall health by providing vitamins (biotin, B5, folic acid, and precursor to vitamin K) to host |
| stomach acid | prevents the growth of many potential pathogens |
| saliva | contains lysozyme and physically washes microbes from teeth |
| body's second line of defense | operates when pathogens succeed in penetrating the skin or mucous membranes; effective against wide variety of pathogens |
| second line of defense is composed of | cells, antimicrobial chemicals, and processes but no physical barriers; many of these originate or are contained in blood |
| some cells and chemicals from first line of defense also | play roles in second line of defense |
| plasma | includes iron-binding proteins transferrin and ferritin which transport and store iron for humans, but they help sequester iron from microbes, some bacteria secrete siderophores to steal iron from body other plasma proteins include complement and antibody |
| leukocytes | defensive blood cells |
| leukocytes are | white blood cells involved in defending body against invaders; granulocytes and agranulocytes |
| granulocytes | basophils, eosinophils, and neutrophils |
| agranulocyte | monocytes, macrophages, and lymphocytes |
| erythrocytes | carry oxygen and carbon dioxide in the blood |
| platelets | involved in blood clotting |
| phagocytosis | process of transporting a solid substance into a eukaryotic cell |
| cells capable of phagocytosis are called | phagocytes |
| 6 stages of phagocytosis | chemotaxis, adhesion, ingestion, maturation, killing, elimination |
| positive chemotaxis | involves the use of pseudopodia to migrate toward microorganisms at the site of infection |
| attractants in chemotaxis include | microbial components and secretions, components of damaged tissues and wbc, and chemotactic factors (defensins, peptides derived from complement, and chemokines) |
| adhesion | attachment through binding of complementary chemicals |
| virulence factors may hinder | adherence |
| opsonization | coating of pathogen with proteins (opsonins) that help increase phagocytosis |
| opsonins | increase the number and kinds of phagocyte binding sites on a microbe's surface |
| ingestion | pseudopodia surround the microbe, which is internalized in a food vesicle called phagosome |
| lysosomes add digestive chemicals | to the maturing phagosome |
| phagosome becomes a | phagolysosome |
| phagolysosome | contains toxic forms of oxygen, ph ~5.5, ~30 different enzymes including lipases, proteases, nucleases, and a variety of others, most pathogens dead within 30 mins, but some contain virulence factors that resist a lysosome's action |
| elimination | digestion is not always complete and phagocytes eliminate remnants via exocytosis, some components are specifically processed and remain attached to the cytoplasmic membrane (role in immune response) |
| nonspecific chemical defenses | augment phagocytosis either by directly attacking pathogens or by enhancing other features of innate immunity |
| nonspecific chemical defenses include | lysozyme, dermcidins, toll-like receptors, NOD proteins, inferferons, and complement |
| interferons | protein molecules released by host cells to nonspecifically inhibit the spread of viral infections |
| interferons cause symptoms like | malaise, muscle aches, chills, headache, and fever often associated with viral infections |
| types of interferons | type 1 and 2 |
| type 1 interferon (alpha and beta) | produced early in viral infections, secreted within hours after infection by viruses, trigger protective steps in neighboring uninfected cells |
| type 2 interferon (gamma) | produced later in the course of infection; also known as macrophage activation factor and is involved in regulating the immune system |
| binding of interferon to interferon recepters on the cytoplasmic membranes of neighboring cells | binding triggers the production of antiviral proteins (AVPs) which remain inactive within these cells, AVP binding to viral nucleic acids (dsRNA) activates |
| activated AVP enzymes are | oligoadenylate synthetase and protein kinase; destroy the protein production system of the cell, cellular metabolism is also affected, and host cell eventually dies |
| complement | set of serum proteins that initially act as opsonins and chemotactic factors, and indirectly trigger inflammation and fever; end result of full complement activation can be the destruction of foreign cells |
| complement can be activated in 3 ways | classical, alternate, and lectin pathway |
| classical pathway | antibodies activate complement |
| alternate pathway | occurs independently of antibodies |
| lectin pathway | mannose attaches to activating molecules called lectins |
| complement enzymes in early events cleave other | complement molecules to form fragments that have different roles in second line of defense |
| C3b | acts as an opsonin |
| C5a | functions as a chemotactic factor |
| C3a, C4a, C5a | inflammatory agents that cause localized vascular dilation, leading to inflammation |
| C3a, C5a | trigger the release of other inflammatory chemicals |
| membrane attack complex (MAC) | end product of full cascade that forms a circular hole in a pathogen's membrane |
| inflammation | general, nonspecific response to tissue damage resulting from a variety of causes (heat, chemicals, uv light, abrasions, cuts, and pathogens) |
| acute inflammation | develops quickly, is short-lived, typically beneficial, and results in the elimination or resolution of whatever condition caused it |
| chronic inflammation | long-lasting, causes damage or even death to tissues, resulting in disease |
| inflammation is characterized by | redness, heat, swelling, and pain |
| inflammation in 2nd line of defense | dilation and increased permeability of blood vessels, migration of phagocytes, tissue repair |
| fever | body temp >37 C, augments the beneficial effects of inflammation |
| side effects of fever | malaise, body aches, and tiredness |
| fever results when | chemicals called pyrogens trigger the hypothalamus to increase the body's core temperature |
| pyrogens include | bacterial toxins, cytoplasmic contents of bacteria released by lysis, antibody-antigen complexes, and pyrogens released by phagocytes that have phagocytized bacteria |
| blood vessels do what when fever progresses | constrict to counteract the process of vasodilation (in inflammation); produces the symptom of chills associated with fever |
| fever continues when | pyrogens are present |
| when pyrogen decreases | thermostat is reset to 37 C and body begins to cool by perspiring, lowering the metabolic rate, and dilating blood vessels in the skin |
| benefits of fevers | enhances the effects of interferons, inhibits the growth of some microorganisms, is thought to enhance the performance of phagocytes, the activity of cells of adaptive immunity, and tissue repair |
| if fever too high | critical proteins are denatured and nerve impulses are inhibited, resulting in hallucinations, coma, and even death |
| first line | skin and mucous membranes |
| second line | phagocytosis, interferons, complement, inflammation, and fever |
| vaccination | application of specific immune response |
| adaptive immunity | a vertebrae's ability to recognize and mount a defense against distinct invaders and their products |
| five attributes of adaptive immunity | specificity, inducibility, clonality, unresponsiveness to self, memory |
| adaptive immunity | involves two main lymphocytes (wbcs) that act against specific pathogens |
| lymphocytes in adaptive immunity | b lymphocytes (cells) and t lymphocytes (cells) |
| b cells | arise and mature in red bone marrow |
| t cells | arise in red bone marrow and mature in thymus |
| b cells carry out antibody immune responses | act against extracellular pathogens and toxins, t cells help regulate and fulfill antibody immune responses |
| cell-mediated immune responses carried out by t cells | often act against intracellular pathogens |
| lymphatic system | the organs, tissues, and cells of adaptive immunity; components constitute a surveillance system that screens the tissues of the body-particularly possible points of entry-for foreign molecules |
| antigens | molecules that trigger adaptive immune responses |
| antibodies | protective proteins secreted by descendants of b cells |
| chemical signals and mediators | coordinate and control a specific immune response |
| lymphatic vessels form | a one-way system that conducts lymph from local tissues and returns it to the circulatory system |
| lymph arises from | fluid leaking from blood vessels into surrounding tissues |
| lymph carries | toxins and pathogens to areas where lymphocytes are concentrated |
| lymph only flows | towards the heart |
| lymph nodes house | leukocytes that recognize and attack foreigners present in the lymph |
| primary lymphoid organs | red bone marrow and thymus |
| secondary lymphoid organs and tissues | lymph nodes, spleen, tonsils, and MALT |
| lymph nodes filter | lymph |
| spleen filters | blood and removes bacteria, viruses, toxins, and other foreign matter from blood |
| MALT includes | appendix; lymphoid tissue of respiratory tract, vagina, urinary bladder, and mammary glands; and Peyer's patches in the small intestine |
| MALT contains | most of the body's lymphocytes |
| antigens | adaptive immune responses are directed against portions of cells, viruses, and even parts of single molecules that the body recognizes as foreign and worthy of attack |
| lymphocytes bind to antigens and | trigger adaptive immune responses |
| properties of antigens | more effective at provoking adaptive immunity with shape, size and complexity |
| body recognizes antigens by 3d shapes | epitopes (antigenic determinants) |
| larger molecules are better | antigens than smaller ones |
| large foreign macromolecules like | proteins and glycoproteins are most effective antigens |
| complex molecules make better antigens too bc | have more epitopes |
| MHC proteins in cytoplasmic membranes function to | hold and position epitopes for presentation to immune cells |
| class I mhc molecules found on | cytoplasmic membranes of all cells expect rbc (all nucleated cells) |
| class II mhc molecules found on | professional antigen-presenting cells (B cells, macrophages, and dendritic cells) |
| if an antigen fragment cannot be bound to an mhc molecule, it | typically does not trigger an immune response |
| before mhc proteins can display epitopes | antigens must be processed |
| processing endogenous antigens (come from a cell's cytoplasm or from pathogens living within the cell) | few molecules of each polypeptide (self and nonself) produced within nucleated cells are broken into small pieces and are loaded onto class I mhc molecules, this complex is then displayed on the cell's cytoplasmic membrane |
| processing exogenous antigens (extracellular sources) | apc (dendritic cells) phagocytizes the invading pathogen and breaks clips its proteins into segments, epitopes are loaded onto class II mhc molecules, this complex is then also displayed on the cell's cytoplasmic membrane |
| t cells | act against body cells that harbor intracellular pathogens and against body cells that produce abnormal cell-surface proteins |
| t cells act directly | against antigens |
| t cells are produced | in red bone marrow and mature under the influence of the thymus |
| t cells circulate | in the lymph and blood and migrate to the lymph nodes, spleen, and peyer's patches (account for 70-85% of all lymphocytes in the blood) |
| t cells maturation | involves the production of ~500,000 copies of a t cell receptor (tcr) on each cell's cytoplasmic membrane |
| types of t lymphocytes | cytotoxic t lymphocyte, helper t lymphocyte, regulatory t lymphocyte |
| cytotoxic t lymphocyte | directly kills cells infected with viruses and other intracellular pathogens, as well as abnormal cells |
| helper t lymphocyte | functions to help regulate the activities of b cells and cytotoxic t cells by providing necessary signals and growth factors (cytokines) |
| helper t lymphocyte factors | th1, th2 |
| th1 | assists cytotoxic t cells and stimulate and regulate innate immunity |
| th2 | function in conjunction with b cells |
| regulatory t lymphocyte | represses adaptive immune responses and prevent autoimmune diseases |
| every t cell has a different shaped antigen-binding site that | recognizes and binds to a complementary shape |
| tcrs only bind epitopes associated with | a mhc protein |
| there are at least | 10^9 different tcrs in your body |
| clonal deletion of t cells | every population of maturing t lymphocytes includes numerous cells with receptors complementary to normal body components (autoantigens) |
| however, the immune system must be tolerant of | self |
| body eliminates self reactive lymphocytes via clonal deletion | lymphocytes are exposed to autoantigens, those lymphocytes that react to autoantigens undergo apoptosis |
| result of clonal deletion is | surviving lymphocytes respond only to foreign antigens |
| this process occurs in the | thymus and takes about 1 week |
| b cells and antibodies found | spleen, MALT, lymph nodes; small % of b cells circulate in the blood |
| major function of descendants of b cells is to | secrete soluble antibodies |
| surface of each b cell contains | b cell receptor (bcr) which is a type of immunoglobulin |
| all bcrs on single b cell are same, but | bcrs of one cell differ from bcrs of all other b cells |
| scientists estimate that each person forms 10^9-10^13 b cells | each with its own bcr |
| when antigenic epitope binds to its unique bcr, | b cell undergoes cell division, giving rise to nearly identical offspring that secrete immunoglobulins into blood or lymph |
| immunoglobulins act against epitope | that is stimulated b cell |
| activated, immunoglobulin-secreting b cells are | plasma cells |
| antibodies are free immunoglobulins and are | similar to bcrs in shape |
| have identical antigen-binding sites and | antigen specificity as bcr of activated b cell |
| five classes of antibodies | IgM, IgG, IgA, IgE, IgD |
| antibody binding to epitope is | central functional feature of antibody immune responses |
| once bound, antibodies function | activation of complement and inflammation, neutralization, opsonization, agglutination, antibody-dependent cytotoxicity |
| two or more IgM antibodies bind to complement protein 1 | begins classical complement pathway |
| IgE binding to epitope and mast cells and eosinophils | triggers the release of inflammatory chemicals |
| neutralization | antibodies can bind to a critical portion of a toxin or can block adhesion molecules on surface of a bacterium or virus |
| toxin cannot function and pathogen cannot adhere to target cell during | neutralization |
| opsonization | changing the surface of an antigen in order to enhance phagocytosis, antibodies act as opsonins (molecules that stimulate phagocytosis) |
| agglutination | numerous antibodies can aggregate antigens together, each antibody can attach to two epitopes at once |
| agglutination causes soluble molecules to precipitate | may hinder the activity of pathogens, increased chance of phagocytosis, increased chance of being filtered by the spleen |
| antibodies coat a target cell and | bind to natural killer cells |
| NK cells lyse target cells by | triggering apoptosis |
| threats confronting the immune system are variable | class involved in the immune response depends on the type of foreign antigens, the portal of entry, and antibody function needed--> 5 different classes of antibodies |
| clonal deletion of b cells | occurs in bone marrow in a manner similar to deletion of t cells; end result is that self-reactive b cells are removed from active b cell repertoire |
| cytokines are soluble regulatory proteins that act as intercellular messages when released by certain body cells | immune system cytokines are secreted by various leukocytes and affect diverse cells |
| cell-mediated immune responses | responds to intracellular pathogens and abnormal body cells |
| body induces cell-mediated immune responses | only against specific endogenous antigens |
| most common intracellular pathogens are viruses | but response is also effective against cancer cells, intracellular protozoa, and intracellular bacteria |
| final result of cell-mediated immune response | cytotoxic t cells kills their targets through one of two pathways; perforin-granzyme pathway, cd95 cytotoxic pathway |
| some ctls become | memory t cells |
| memory t cells | persist for months or years in lymphoid tissues |
| memory t cells become function | immediately upon subsequent contacts with an epitope-mhc I protein complex matching its tcr; produces cytotoxic t cell clones that recognize the offending epitope |
| benefit of memory t cells | need fewer regulatory signals nd become functional immediately, response is much more effective (memory response) due to the number of memory t cells that respond |
| body mounts antibody immune responses against | antigens of exogenous pathogens and toxins |
| activates only in response to specific pathogens | antibody immune responses |
| two types of antibody immune responses | t-independent antibody and t-dependent antibody immunity |
| t-independent antibody immunity (no assistance from Th cell) | antigens consist of many identical, repeating epitopes (polysaccharides), weak immunity that disappears quickly and induces little memory, stunted in children |
| t-dependent antibody immunity (requires assistance from Th2 cell) | antigens lack numerous, repitive, and identical epitopes, involves a series of interactions among apcs, th2 cells, and b cells, all of which are mediated and enhanced by cytokines |
| t-dependent humoral immunity with clonal selection | most members of a clone become plasma cells; IgM-->IgG, IgA, or IgE; are short lived cells that die within a few days of activation, though their antibodies persist for several weeks and their descendants persist for years |
| small percentage of cells produced during b cell proliferation survive as b memory cells (long-lived cells that have bcrs complementary to the specific epitope that triggered their production) | memory cells and establishment of immunological memory |
| long-lived cells that persist in the lymphoid tissue | survive more than 20 years |
| available to initiate antibody production if | same epitope is encountered again |
| adaptive immunity acquired | during an individual's life |
| naturally acquired active immunity | getting flu |
| naturally acquired passive immunity | baby gets antibodies from mother's breast milk |
| artificially acquired active immunity | vaccine (antigens) |
| artificially acquired passive immunity | receiving antibodies from previous patient |
| vaccination is most | efficient and cost-effective method of controlling infectious diseases |
| many infectious diseases are nw | controlled or even eliminated due to vaccination |
| the administration of antibodies can | further reduce incidence of disease and prevent death |
| active immunization | involves administering antigens to a patient so that the patient actively mounts a protective immune response |
| passive immunotherapy | a patient acquires temporary immunity through the transfer of antibodies formed by other individuals or animals |
| children who recovered from | smallpox in china did not contract disease again |
| chinese infected you children with | smallpox scabs in variolation |
| variolation | spread to england and america but was stopped due to risk of death |
| edward jenner discovered | vaccination by inoculating crusts from a person infected with cowpox (related but very mild disease) |
| practice of transferring antibodies was developed when | it was discovered vaccines protected through the action of antibodies |
| by 1900s, there were vaccines that significantly | reduced the # of cases of many infectious diseases |
| hoping for worldwide eradication of | polio, measles, mumps, and rubella |
| variety of social, economic, and scientific problems prevent | vaccines from reaching all those who need them; 3 mill children die each year from vaccine-preventable infectious diseases |
| in all active immunizations | pathogen is altered or inactivated so it is less likely to cause illness |
| not all types of vaccines are equally | safe or effective |
| effectiveness of vaccines is determined | by checking the antibody titer (concentration of IgG and IgM) in the blood |
| types of active immunization | attenuated (modified live) vaccines, inactivated (killed) vaccines, toxoid vaccines, combination vaccines, and vaccines using recombinant gene technology |
| attenuated (modified live) vaccines | use pathogens that have reduced virulence so they do not cause disease (attenuation) |
| attenuated vaccines cause | mild infections but no serious disease under normal conditons |
| attenuated vaccines contain | active microbes that stimulate a strong immune response due to the large number of antigen molecules that are available (antibody and cell-mediated immunity) |
| attenuated vaccinated individuals can infect | those around them, providing contact immunity; very effective |
| attenuated vaccination can be | hazardous bc modified microbes may retain enough residual virulence to cause disease in immunosuppressed people |
| pregnant women should not receive | attenuated vaccines |
| attenuated vaccines can revert to | wild type or mutate to a form that causes disease |
| inactivated (killed) vaccines | two types-both are safer than live vaccines bc cannot replicate, revert, mutate, or retain residual virulence |
| types of inactivated vaccines | whole agent vaccines and subunit vaccines |
| whole agent vaccines | deactivated but whole microbes |
| subunit vaccines | antigenic fragments of microbes |
| inactivated vaccines are antigenically weak bc | microbes don't replicate and don't provide many antigenic molecules to stimulate the immune response |
| higher doses or boosters are required for full immunity in | inactivated vaccines |
| inactivated vaccines contain | adjuvants (chemicals added to increase the effective antigenicity) |
| no contact immunity is stimulated | nonantigenic portions occasionally stimulate painful inflammatory response in some |
| inactivated vaccines stimulate | antibody immune response (exogenous antigens) |
| toxoid vaccines | sometimes more efficient to induce an immune response against bacterial toxins than against cellular antigens, chemically or thermally modified toxins used to stimulate active immunity |
| toxoid vaccines require | multiple childhood doses and reinoculations every 10 years bc possess few epitopes |
| combination vaccines | combine antigens from several attenuated and inactivated pathogens and toxoids that are administered simultaneously (MMR) (pentacel) |
| vaccines using recombinant gene technology | researches seeking to make new vaccines that are more effective, cheaper, and safer and to make new vaccines against pathogens that have been difficult to protect against |
| variety of recombinant dna techniques can be used to make improved vaccines | selectively delete virulence genes, produce large quantities of very pure antigens for use in vaccines, live recombinant vaccines, dna vaccines |
| herd immunity | protection provided all individuals in a population due to the inability of a pathogen to effectively spread when a large proportion of people (>75%) are immune |
| mild toxicity is most common in vaccines | pain at injection site is more common with whole agent vaccines that contain adjuvant, rare cases toxicity may result in general malaise and high fever |
| risk of anaphylactic shock | with vaccines |
| allegations that certain vaccines against childhood diseases cause or trigger autism, diabetes, and asthma | research has not substantiated these allegations, modern vaccines are much safer than those in use even 10 years ago |
| passive immunotherapy | used to provide immediate protection against recent infection or a ongoing disease, but does not require body to mount a response |
| passive immunotherapy is derived from | human blood plasma donors or large animals intentionally exposed to a pathogen of interest |
| limitations of passive immunotherapy | can trigger allergic reactions (serum sickness), antibodies are degraded relatively quickly (protectio not long lasting), body does not produce memory b cells, so patient is not protected against subsequent infections |
| hypersensitivity | any immune response against a foreign antigen that is exaggerated beyond the norm |
| types of hypersensitivities | type i (immediate), type ii (cytotoxic), type iii (immune complex-mediated), type iv (delayed or cell-mediated) |
| type i (immediate) aka allergies | localized or systemic reaction that results from the release of inflammatory molecules in response to an antigen, develops within seconds or minutes following exposure to an antigen |
| antigens that stimulate type 1 | allergens |
| type 1 reactions occur in 2 steps | sensitization upon initial exposure to an allergen and degranulation of sensitized cells |
| sensitization upon initial exposure to an allergen | IgE produced rather than IgG, IgE binds strongly to mast cells, basophils, and eosinophils |
| degranulation of sensitized cells | release of potent inflammatory chemicals |
| mast cells | distributed throught the body in connective tissue, have granules that contain inflammatory chemicals; degranulation releases histamine, kinins, proteases, leukotrienes, and prostaglandins |
| basophils | least numerous leukocyte in the blood, have granules that contain inflammatory chemicals, degranulate like mast cells when allergens are encountered |
| eosinophils | mast cell degranulation can trigger the release of eosinophils from the bone marrow, in the bloodstream can degranulate, release large amounts of leukotrienes, increases severity of hypersensitivity response |
| signs of LOCALIZED allergic reactions | usually mild and localized, site of reaction depends on portal of entry, inhaled allergens may cause hay fever, small inhaled allergens may reach lungs and cause asthma, some allergens may cause inflammation of skin (hives or urticaria) |
| signs of SYSTEMIC allergic reactions | many mast cells may degranulate at once and release large amounts of histamine and inflammatory mediators, acute anaphylaxis or anaphylactic shock can result, clinical signs of suffocation, treated promptly with epinephrine, causes from bee stings/foods |
| diagnosis of type 1 | based on detection of high levels of allergen-specific IgE, test referred to as ImmunoCAP Specific IgE blood test, CAP RAST, or Pharmacia CAP, can also diagnose using skin tests |
| prevention of type 1 | identification/avoidance of allergens, elimination diet, immunotherapy (allergy shots) but must be administered in series of injections of dilute allergen, repeated every 2-3 years, and not effective in treating asthma |
| treatment of type 1 | drugs that counteract inflammatory mediators (antihistamines neutralize histamine), asthma with glucocorticoid and bronchodilator, epinephrine for anaphylaxis |
| epinephrine | relaxes smooth muscle, reduces vascular permeability, used in emergency treatment of severe asthma and anaphylactic shock |
| type ii (cytotoxic) | results when cells are destroyed by immune response (combined activities of complement and antibodies), component of many autoimmune diseases |
| examples of type 2 | destruction of blood cells following an incompatible blood transfucion (ABO system and Transfusion reactions), destruction of fetal rbc (RH system and hemolytic disease of newborn) |
| abo system | blood group antigens are surface molecules on rbcs, each persons rbc have a antigen, b antigen, both, or neither |
| transfusion reactions | result if individual receives differnt blood type, donor's blood group antigens may stimulate production of antibodies in recipient, destroying transfused cells (can be life-threatening) |
| recipient has preexisting antibodies to foreign blood group antigens | immediate destruction of donated blood cells can occur, severe signs and symptoms occur |
| recipient has no preexisting antibodies to foreign blood group antigens | transfused cells initially circulate and function normally, eventually recipient's immune system mounts a primary response against foreign antigens and destroys them, gradual reaction |
| Rh antigen | common to rbc of humans and rhesus monkeys; ~85% humans Rh+ |
| if rh- woman carries rh+ feuts | antibody immune response may be initiated against fetal cells |
| in subsequent pregnancy | fetus may be at risk for hemolytic disease |
| administration of anti-rh immunoglobulin (RhoGAM) | reduced cases of hemolytic disease of newborn |
| type iii (immune complex-mediated) | caused by formation of immune complexes (antibody-antigen); normally removed from body via phagocytosis, small immune complexes become trapped in organs, joints, and tissues; complement activated resulting in inflammation and tissue damage |
| type 3 can cause | localized reactions (hypersensitivity penumonitis and glomerulonephritis) and systemic reactions (systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA)) |
| hypersensitivity penumonitis | inhalation of antigens deep in lungs stimulates production of antibodies (sensitization step), subsequent inhalation of same antigen stimulates the formation of immune complexes (activates complement) |
| glomerulonephritis | immune complexes circulating in the bloodstream are deposited in walls of glomeruli, damage to glomerular cells impedes blood filtration, kidney failure/death result |
| rheumatoid arthritis (ra) | b cells secrete IgM that binds to IgG molecules; immune complexes deposited in the joint, results in release of inflammatory chemicals, joints begin to break down and become distorted (damage more severe); treated with anti-inflammatory drugs |
| systemic lupus erythematosus (SLE) | autoantibodies against nucleic acid, especially dna, result in immune complex formation, immune complexes deposit in glomeruli and skin |
| other autoantibodies occur | against rbc (hemolytic anemia), platelets (bleeding disorders), lymphocytes (immune reactivity), and muscle cells (muscle inflammation and heart damage) |
| treatment for sle | immunosuppressant drugs reduces autoantibody formation, glucocorticoids reduce inflammation |
| type iv (delayed or cell-mediated) | inflammation begins 12-24 hrs after contact with certain antigens, resulting from actions of antigen, antigen-presenting cells, and t cells |
| type 4 | delay reflects the time it takes for macrophages and t cells to migrate to and proliferate at the site of antigen |
| examples of type 4 | tuberculin response, allergic contact dermatitis, graft rejection, graft-vs-host disease, donor-recipient matching and tissue typing |
| tuberculin response | skin of person exposed to tuberculosis or vaccine reacts to injection of tuberculin beneath skin; used to diagnose contact with antigens of m. tuberculosis; |
| reactions to tb test | no response when individual has not been infected or vaccinated, red, hard swelling develops in individuals currently or previously infected or immunized 24-72 h after injection; response mediated by memory t cells that cause slow developing inflammation |
| allergic contact dermatitis | cell-mediated immune response resulting in intensely irritating skin rash, triggered by chemically modified skin proteins that body regards as foreign; in sever cases: acellular, fluid-filled blisters develop; |
| allergic contact dermatitis caused by | poison ivy, formaldehyde, cosmetics, dyes, drugs and metal ions, chemicals to produce latex; treated with corticosteroids |
| graft rejection | rejection of tissues or organs that have been transplanted; perceived as foreign by recipient undergo rejection; normal immune response against mhc proteins present on graft cells; likelihood of rejection depends on degree of graft being foreign (type) |
| graft-vs-host disease | donated bone marrow cells regard patients cells as foreign |
| donor and recipient differ in mhc class i molecules | grafted t cells attack all of recipients tissues and produce lesions in skin and intestine |
| donor and recipient differ in mhc class ii molecules | grafted t cells attack recipients apcs which lead to immunosuppression and leaves recipient vulnerable to infection; can be limited by immunosuppressive drugs |
| donor-recipient matching | mhc compatibility bw donor and recipient is difficult due to high degree of variability; closer donor and recipient are related, smaller difference is in mhc; preferable that grafts donated by sibling/parent |
| tissue typing | used to match donor and recipient, examine wbc of potential graft recipients to determine what mhc proteins they have; donor organ becomes available also typed, recipient whose mhc proteins most match is chosen to receive graft |
| which complement pathway is useful during early stages of infection before adaptive immune response becomes functional? | alternate |
| the complement system and its products play important roles in overall innate (nonspecific) immune response. Of options below, which is not affected by the complement system? | interferon production |
| which of the following would be presented on mhc class i proteins? | a viral peptide inside a host cell |
| a t cell and tcr recognize two components. what are these? | mhc protein and processed antigen |
| what are the cells that recognize mhc class i plus processed and presented antigen? | t cytotoxic cells |
| what are the lymphocytes that physically kill infected host cells in the cells in the cell mediated response? | ctls |
| what types of infections would a personn born without t cytotoxic cells have difficulty responding to? | endogenous |
| what types of infections would a person suffer from if he/she/they were unable to produce mhc ii proteins? | exogenous |
| which of the following explains why IgG is produced so much faster in the secondary response as compared to the primary response? | bc memory cells were produced during primary response |
| early in pandemic, one method of treating those infected with SARS Cov 2 was to infuse them with antibodies obtained from someone who had previously recovered from COVID. What type of immunity was provided to the sick patient thru this process? | artificially acquired passive immunity |
| about one in every 750,000 children who received the first dose of the live opv experienced vaccine associated paralytic poliomyelitis. Bc of this, opv was replaced w inactivated version. which explains why some children developed polio after getting opv? | virus in vaccine reverted to wild-type strain |
| contact immunity may result following the administration of which type of vaccine | attenuated whole organism |
| thee are 2 types of flu vaccines available, inactivated and live attenuated. In terms of immune response generated in vaccinated individuals, which would be most effective and why? | live vaccine bc it provides both antibody and cel-mediated immunity |
| when a person has been exposed to rabies, he/she receives both HRIG injected near infection site as well as rabies vaccine. What does this strategy represent? | passive immunotherapy combined with active immunization |
| you want to create vaccine in which large # of antigen molecules will be available to stimulate an immune response and which can be administered in single dose (rather than multiple boosters). focus efforts on developing what type of vaccine? | attenuated (live) whole organism vaccine |
| cell-mediated immunity acts against | endogenous (intracellular) antigens |
| cell-mediated immunity involves what type of lymphocytes | t cells (Tc cells) |
| cell-mediated immunity is activated by | Tc recognizes MHC I plust antigenic determinant & becomes activated, cannot move past this step w/o assistance |
| cell-mediated immunity uses TH cells | TH recognized MHC II plus antigenic determinant on APC and differentiates into TH I and TH 2 cells |
| cell-mediated immunity uses what T helper | TH I |
| cell-mediated immunity is fully activated when | TH I secretes cytokines to cause activated Tc to go thru clonal expansion and differentiation to form cytotoxic T lymphocytes (ctls) |
| cell-mediated immunity products created | ctls |
| cell-mediated immunity activity of products | ctls kill any cell displaying the specific antigenic determinant in conjunction w MHC I protein |
| t dependent antibody-mediated immunity acts against | exogenous (extracellular) antigens |
| t dependent antibody-mediated immunity involves what type of lymphocytes | b cells |
| t dependent antibody-mediated immunity is activated by | b cell acts as an APC to present antigenic determinant along w MHC II |
| t dependent antibody-mediated immunity uses TH cells | TH recognizes MHC II plus antigenic determinant on APC and differentiates into TH I and TH2 cells |
| t dependent antibody-mediated immunity uses what T helper | TH 2 |
| t dependent antibody-mediated immunity is fully activated when | TH 2 binds to activated b cell and causes the b cell to undergo clonal expansion and differentiation to from plasma cells |
| t dependent antibody-mediated immunity products created | plasma cells |
| t dependent antibody-mediated immunity activity of products | antibodies participate in: activation of classical complement pathway, inflammation, neutralization, agglutination, ADOC |
| an accident victim receives blood transfusion, shortly after begins having difficulty breathing, fever, and nausea/vomiting. what is the interpretation of these events? | blood transfusion was mismatched and recipient had previously been exposed to the foreign blood group antigens |
| an agricultural worker experiences difficulty breathing which gets worse. tests show inflammation and damage to lung tissue, but IgE antibodies and granulocytes are normal. what disorder are these signs and symptoms consistent w? | type iii (immune complex-mediated) hypersensitivity |
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