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Chap 26 - Innate Imm
Innate Immunity: Broadly Specific Host Defenses
| Question | Answer |
|---|---|
| immunity is | the ability of an organism to resist infection |
| innate immunity is (specific/nonspecific) | innate immunity is NONSPECIFIC |
| what is the function of innate immunity | the noninducible ability to recognize and destroy an individual pathogen or its products |
| innate immunity (does/does not) require previous exposure to a pathogen or its products | innate immunity DOES NOT require previous exposure to a pathogen or its products |
| adaptive immunity is (specific/nonspecific) | adaptive immunity is SPECIFIC |
| this is the *aquired* ability to recognize and destroy a particular pathogen or its products | adaptive immunity |
| adaptive immunity is dependent on | previous exposure to a specific pathogen or its products |
| define specificity | the ability of the adaptive immune system to attack and destroy a specific pathogen |
| adapted immunity is directed towards | and individual molecular component of a pathogen |
| another word for antigen | pathogen |
| the primary effectors in the innate immunity | phagocytes |
| name the three main white blood cells that are part of innate immunity | dendritic cells, neutrophils, macrophages |
| this type of immunity has no memory after exposure | innate immunity |
| (innate/adaptive) immunity has a rapid response that can respond within several hours; (innate/adaptive) immunity response requires a few days | INNATE immunity is rapid, ADAPTIVE immunity can take days |
| what are the primary effector cells that for the adaptive immune system | Lymphocytes (B and T) |
| Antibodies come from | plasma cells |
| for an active infection, what adaptive immunities help fight the infection | antibodies and cytotoxic T cells |
| after exposure to an infection, how is adaptive immunity kept up | B-Cells and Memory T-Cells |
| the Normal microbiota help with pathogen resistance, ho | competitive exclusion (particularly in the skin and gut) |
| (not a question) the ability of a microbe to cause disease varies between species (I.e. variable sensitivity to rabies, failure of diseases to pass between cold and warm blooded animals) | |
| tears and other bodily secretions carry ______________ and dissolves bacterial walls | lysozyme |
| these anatomical structures in the nasopharynx, and trachea help to remove particles | cilia |
| what is the function of mucus lining the trachea walls | to trap/suspend the microorganisms |
| there are several important functions of skin, what are they | 1) physical barrier, 2) production of antimicrobial fatty acids, 3) production of antibacterial peptides, 4) host normal microbiota that help inhibit infection |
| several things in the lungs help prevent infection, what are they | mucus, antibacterial peptides, and roaming phagocytes |
| how do epithelial cells through out the body prevent infections, | they have tight junctions that inhibit pathogens from entering |
| in the urinary tract, what helps prevent infection | flushing of the bladder |
| (not a question) different pathogens invade different tissues and routes of infection are crucial (tetanus = wounds, Salmonella = ingestion) | |
| what is the pathogen for Acquired immunodeficiency syndrome (AIDS) | HIV (Human immunodeficiency virus) |
| what does HIV/AIDS infect | helper T-lymphocytes |
| Botulism is caused by _________________ and infects the ___________________ | Clostridium botulinum; Motor End Plate |
| Vibrio cholerae is commonly called ____________________ and infects the _________________ | Cholera; Small intestine epithelium |
| Dental Caries are caused by __________________ and infect ___________________ | Streptococcus mutans, S. sobrinus, S. mitis; oral epithelium |
| Cprynebacterium diphtheriae causes | Diptheria |
| Diptheria infects ______________________ | throat epithelium |
| Gonorrhea is caused by ____________________ and infects ______________________ | Neisseria gonorrhoeae; Mucosal epithelium |
| Influenza is caused by ______________________ and infects _________________ | Influenza A & B virus; respiratory epithelium |
| Malaria is caused by _______________ and infects _____________________ | Plasmodium spp.; Blood (erythrocytes) |
| Pyelonephritis is caused by _________________ and infects ____________________ | Proteus spp.; Kidney medulla |
| Spontaneous abortions in cattle is caused by ____________________ and infects _____________ | Brucella abortus; Placenta |
| Tetanus is caused by ______________________ and infects __________________________ | Clostridium tetani; Inhibitory neurons |
| describe the lymphatic system | a separate circulatory system that drains lymph fluid from extravascular tissues |
| in what location of the circulatory system do leukocytes and solutes pass from the blood to the lymphatic system | capillary beds |
| the lymph nodes contain high concentrations of | lymphocytes and phagocytes |
| leukocytes (including phagocytes and lymphocytes) make up only _____________________ percent of the blood cells | 0.1% |
| _________________________ influence the development of stem cells | Cytokines |
| what his whole blood composed of | plama (liquid), its protiens, other solutes, and cells |
| what is serum | the liquid portion of the blood that is not cells or clotting proteins (DOES contain antibodies) |
| Leukocytes (are/are not) nucleated | Leukocytes ARE nucleated |
| ___________________ are specialized leukocytes involved exclusively in the adaptive immune response | Lymphocytes |
| name the two types of lymphocytes | T-Cells and B-cells |
| where do T Cells originate and mature | T Cells originate in the red bone marrow, and mature in the thymus |
| where do B cells originate and mature | B cells originate and mature in the red bone marrow |
| the primary lymphoid organ(s) is(are) | bone marrow and thymus |
| Myeloid cells are derived from | myeloid precursor cell |
| what are the two categories that a myeloid cell can be divided into | antigen-presenting cells (APCs) and granulocytes |
| what is the function of antigen presenting cells | engulfing, processing, and presenting antibodies to lymphocytes |
| what white blood cell types are antigen-presenting cells | monocytes, macrophages, and dendritic cells |
| what are the functions of granulocytes | contain toxins or enzymes that are released to kill target cells |
| what types f white blood cells are granulocytes | neurtophils, basophils, and eosinophils |
| lymphoid stem cells produce | T Cells, B Cells, NK (natural killer) cells |
| Each lymphocyte produces a unique protein that interacts with a single foreign antigen. what is it for the T Cells? what is it for the B Cells? | T Cells = T Cell receptors (TCRs); B Cells = antibodies/immunoglobulins (Ig's) |
| what is the invasion phase of an infection | the ability of a pathogen to enter host cells or tissue, multiply, spread, and cause disease |
| _______________________ triggers the recruitment of a large number of phagocytes | tissue damage |
| what structure(s) release cytokines | resident leukocytes and damaged tissue cells |
| cytokines allow for | communication between white blood cells |
| the release of __________________ and ______________________ draws macrophages and neutrophils to the area as they leave the circulation | cytokines and chemokines |
| what is extravasion | when macrophages and neutrophils leave circulation |
| what are Pathogen-associated molecular patterns (PAMP's) | certain structures /molecules on pathogens that are not present of the host cell |
| what are some examples of PAMPs | peptidoglycan, flagellin, and double stranded RNA |
| what are pattern recognition receptors | membrane-bound/soluble proteins on leukocytes that recognize PAMPs |
| upon encountering a pathogen associated molecular pattern (PAMP) ______________________________ will send a signal to the nucleu | Toll-like receptors (TLR) |
| all toll-like receptors have analogous mechanisms for activating __________________ immunity | TLR activate INNATE immunity |
| once TLR is activated in a leukocyte will start a _________________________ cascade to transmit the activation signal to the nucleus | phosphorylation |
| __________________ are enzymes that regulate biological activity by adding Phosphate (P) from ATP to specific amino acids | Kinases |
| _____________________ is a key transcription factor that is activated in many different pathways during signal transduction in phagocytes | NFkB |
| what is phagocytosis | when a phagocyte engulfs a pathogen upon recognition of PAMPs by the Toll-like Receptors on phagocytes |
| when does a phgosome occur | when the pathogen is held in a membrane bound vesicle immediately after being engulfed by a phagocyte |
| what is a phaygolysosome | when a phagosome and lysosome combine |
| in what cellular structure do phagocytes produce toxic reactive oxygen intermediates that kill a pathogen | phagolysosome |
| name the some types of bacteria that are known to survive in a phagolysosom | Mycobacteria tuberculosis (Tuberculosis) and Streptococcus pyogenes |
| Tuberculosis produces ___________________ to neutralize singlet oxygen in a phagolysosom and has a waxy cell wall that absorbs free radicles | cartenoids |
| This pathogen lives and divides in phagocytes | Mycobacteria tuberculosis |
| Streptococcus pyogenes produces ______________________ which kill white blood cells | leukocidins |
| dead white blood cells are found in _____________ | pus |
| what is the benefit of having a capsule | it is difficult for a phagocyte to engulf a capsule; however antibodies can react with this (which is partly why vaccines are important) |
| what is inflammation | nonspecific reaction to noxious stimuli |
| what are some signs and symptoms of inflammation | redness, swelling, pain, and localized heat (at site of infection) |
| what proteins draw WBC's to the site of inflammation | cytokines and chemokines |
| describe an effective inflammatory response | limits tissue damage, destroys damaged cells and pathogens |
| describe an uncontrolled inflammation | can results in considerable damage to healthy tissue and key organs (i.e. brain and lungs) |
| what causes a fever | certain cytokines (particularly IL-1) |
| fever-causing cytokines are called | pyrogens |
| why are fevers beneficial | the increase the blood circulation rate, which allows leukocytes to get to the site of the infection faster, some pathogens cannot tolerated the heat |
| name the molecules that are present in fevers and help sequester Iron to keep it away from growing pathogens | transferrins |
| Systemic (widesread) inflammation can lead to | shock, increased vascular permeability, decreased blood pressure, and multiple organ failure/damage |
| why is gram-negative bacteria particularly dangerous | they contain Lipopolysaccharides, which trigger a proinflammatory cytokine response (which can stimuate/enhance the inflammatory response) |
| what can lead to a cytokine storm | LPS from gram-negative bacteria that can trigger a proinflammatory cytokine response |
| the ________________ system is a set of circulating =, inactive proteins that are sequentially activated in response to a pathogen | complement system |
| in the classical pathway of the compliment system begins when | antibodies bind to a pathogen, C1 binds to the antibodies and begins to cleave C2 and C4 |
| in the alternative pathway of the compliment system begins when | factor B, factor P (properdin), and factor D bind to the bacteria (specifically LPS), which cleaves C3 |
| in the lectin pathway of the compliment system begins when | lectins bind to carbohydrates, then cleaves to C2 and C4 |
| in the classical pathway, after C2 and C4 are cleaved, what happens | C2a-C4b combine to make C3 convertase |
| what does C3 convertase (C2a-C4b) do | cleaves C3 |
| after C3 has been cleaved what does C3b do | binds to the target cell, this coating helps make it easier to the phagocytes to engulf it, or it will attach to a C3 convertase |
| after C3 has been cleaved what does C3a do | diffuses into the surrounding area and serves as a chemoattractant |
| what is opsonization | when C3b covers the outside of a pathogen |
| when C3 convertase (C2a-C4b) binds to C3b | the C3 convertase cleaves C5 |
| after C5 is cleaved what happens to C5a and C5b? | C5a is released and C5b binds to the cell |
| what is the Membrane attack complex | when C5b binds to the cell |
| what is the end result of all the pathways in the compliment system | 1) direct attack (via Membrane attack complex), 2) recruitment of phagocytes (C5a and C3a), 3) opsonization (C3b) |
| what makes the Mannose-binding lectin (MBL and alternative pathways different from the classical pathway | they relay on innate mechanisms rather than antibodies to activate the compliment system |
| some chemoattractants (C5a and C3a) are considered __________________, because they can lead to immune over-activation | anaphylatoxins |
| natural killer cells are _________________ | cytotoxic lymphocytes |
| natural killer cells attack body cells that do NOT display ____________ on their plasma protein | Major Histocompatibility Complex I |
| if a natural killer cell targets a host cell with a stress protein, we can likely assume that that cell is infected with | either a virus or has become cancerous |
| what is a granzyme | an enzyme that induces programmed cell death (apoptosis) |
| perforin is | chemically and functionally similar to C9, it pokes holes (or perforates) the target membrane |
| interferons are | small cytokines that are produced by virus-infected cells, they serve as a warning system, |
| how do interferons work on a neighboring cell | interferons stimulate the antiviral proteins that attack the DNA/RNA of an incoming virus |
Created by:
kandriot
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