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Immune System ch21
the immune system
| Question | Answer |
|---|---|
| Innate Defenses | non specific |
| adaptive defenses | specific |
| innate(non specific) | skin intact; mucosal surfaces; associated with secretions. (1st line of defenses) |
| intact skin | mechanical barrier; -sweat, sebum= acidic |
| stomach | acid, protein-digesting enzymes |
| saliva, tears | antibacterial compounds |
| urine, vaginal secretions | acidic |
| hairs, cilia, mucus | trap organisms |
| what are other non specific defenses (2nd line of defense) | cells and mechanisms |
| cells | neutrophils, macrophages,eosinophils, natural killer cells |
| cells and mechanisms (2nd line of defense) | cells inflammation antimicrobial proteins fever |
| neutrophils | phagocytes, engulf and digest; often 1st on the scene; they secrete defenses(antibiotic kills both bacteria and neutrophils |
| macrophages | phagocytes; develop from monocytes; travel through tissues as well as reside in various locations |
| eosinophils | weakly phagocytic; help kills parasitic worms with release of destructive materials from cytoplasmic granules |
| natural killer cells (NK) | large, granular lymphocytes which poke holes in lyse and kill a variety of infected or cancerous cells by recognizing abnormalities (not phagocytic) |
| Inflammation | -swelling -pain -redness -heat |
| benefits of inflammation | prevents spread of pathogens disposes of cell debris and pathogens sets the stage for repair process |
| during inflammation, what sort of chemicals release in the injured tissues? | histamine, kinins, prostaglandins, complement, etc |
| during inflammation, what happens to vasodilation and permeability of capillaries? | they both increase |
| Edema | the increase in fluid accumulation; swelling; it presses on nerve endings and causes pain |
| swollen area may be immobilized (impaired of function) | -forced to rest area -dilution of toxins -more oxygen to area -clotting proteins help wall off area |
| inflammatory process (esp.chemicals) also enhances: | Chemotaxis leukocytosis |
| chemotaxis | attraction of macrophages and neutrophils |
| leukocytosis | injured cells release leukocytosis inducing factor; promotes neutrophil release from red bone marrow |
| Antimicrobial proteins | -Complement -Interferons |
| Complement | is a group of at least 20 plasma proteins; plays a role in both specific and non-specific defenses a series of enzymatic reactions that end in a 5-protein MAC (membrane attack complex) |
| What creates a hole in target by lysing it and also acts as a chemotactic agent; promotes phagocytosis (opsonization) | Complement |
| opsonization | enhancement of phagocytes |
| Interferons | small proteins that are released by virus-infected cells to nearby uninfected cells; these will be taken up and incorporated and will interfere with viral replication |
| what is a systemic response; higher resetting of body thermostat | Fever |
| Why do we get Fevers | response to pyrogens- released by macrophages and other leukocytes exposed to certain pathogens |
| What are 2 benefits of Fevers | increase iron and zinc conservation by liver (bacteria need these) increase metabolic rate of cells overall (speeds up repair) |
| 3rd line of Defense | immune response (adaptive defenses) |
| what are 3 aspects to the immune response (adaptive defenses) | 1) antigen specific 2) systemic 3) has memory |
| the 2 major devisions of the immune response (adaptive defenses) are: | 1) humoral- handled by b-cells 2) cell mediated-handled by t-cells (cell to cell combat) |
| "foreign" material; usually a large, complex protein or polysaccharide | antigen |
| usually what are immune system responds to-> specific sites on an antigenic molecule | antigenic determinants |
| a specific location on a molecule that is recognized by a specific lymphocyte. there may be 100s of such sites on a single foreign molecule(antigen is multivalent | specific site on a antigenic molecule |
| complete antigens | 1) reactivity 2) immunogenicity |
| reactivity | ability to interact with a cell or other component of the immune system |
| immunogenicity | the ability to stimulate specific lymphocytes and trigger antibody formation |
| They are REACTIVE but NOT immunogenic- they evoke a response only when attached to our own proteins (e.g allergy) | Haptens (incomplete antigen) |
| Basis for self recognition (self antigens) | Classes of cell surface proteins, coded for by genes of the major histocompatibility complex (MHC proteins) |
| Class I | MHC proteins-found on a regular body cells' surfaces |
| Class II | MHC proteins- found on the surfaces of mature immune system cells |
| MHC restriction | Class I MHC proteins- signal cytotoxic t-cells Class II MHC proteins- signal helper t-cells |
| 3 crucial cell types for self recognition | t-cells: cell mediated immunity b-cells: humoral immunity macrophages: help in both specific and non specific defenses (as they act as APC's..antigen presenting cells |
| APC's | Engulf antigen, incorporate and display portion of it coupled to the cell-surface self protein (MHC) of its membrane then present it to immune system cells for recognition and action |
| Immunocompetence | genetically determined pre-programmed before meeting antigens |
| invading antigens will... | evoke a response only from t or b cells programmed to respond to it. some will never meet the antigen for which they are programmed |
| B and T cells start out as identical immature lymphocytes, what happens to them when they are competent? | Each cell has a unique receptor for 1 antigenic determinant on its surface |
| 2 places where the t and b cells mature and gain immunologic competence | 1) thymus - t-cells 2) bone marrow - b-cells |
| what happens to those cells with the best abilities to attack foreign materials and have a weak reaction to self antigens | they are retained |
| what happens to those cells with a strong antiself reaction | they are weeded out and destroyed |
| B-cells | Humoral response |
| antigen challenge: | first introduction of a B-cell to its antigen (usually in the spleen or lymph node) |
| the second step to humoral response | surface receptors on b-cell bind to antigenic determinant (several can vind at same time) B cell is activated* |
| the third step to humoral response | antigen-receptor complex is endocytosed |
| the fourth step to humoral response | this triggers Clonal Selection |
| clonal selection | b-cells grow rapidly and multiply identical copies of itself (a clone) |
| the fifth step to humoral response | Most of the clones become plasma cells -secreting antibodies(2000 molecules per second) - 4-5days then die Some become memory b-cells rapid, powerful response to any subsequent exposure (2nd response: anamnestic response) |
| active Immunity | requires body to mount an immune response |
| naturally active immunity | gets infected; b-cells mount a response=meet antigen and respond to challenge |
| artificially active immunity | vaccines; introduced to antigen and body responds |
| passive immunity | doesn't require the body to mount immune response; but receive preformed antibodies |
| naturally passive immunity | across placenta; in breast milk |
| artificially passive immunity | antivenins (snake bites); gamma globulins (hepatitis); botulism, rabies, tetanus |
| antibodies are proteins which are made up of | 4 amino acid chains 2 heavy= 400 a.a 2 light= 200 a.a |
| the proteins fall into 1 of 5 classes, based on a portion of the molecule which has identical amino sequence for all antibodies within that class..this is which region? | the Constant Region |
| one part of the molecule is unique and specific for individual antigenic determinants..it is which region? | the variable region |
| all antibodies have: | an antigen binding site a complement binding site a macrophage binding site |
| Antibodies DO NOT kill directly | True |
| *Antibody Classes (immuneglobins)* | IgD IgM IgG IgA IgE |
| IgD | attach to b-cells; b-cell activation, enhance antibody production |
| IgM | promotes agglutination of microbes and helps activate complement |
| IgG | most abundant and diverse class; main antibody of primary and secondary responses; enhances phagocytosis by complement and fixations; able to cross the placenta |
| IgA | found in body secretions; also associated with mucosal surfaces and prevents pathogen attachment |
| IgE | associated with basophils; causes cells to release histamine- involved in inflammation and allergic responses; helpful to eosinophils |
| 4 mechanisms of antibody action | neutralization- mask dangerous parts of bacterial exotoxins, viruses agglutination- cell bound antigens precipitation- soluble antigen complement-fixation and activation of complement formation |
| cell mediated immunity | T-cells |
| three major types of cell mediated immunity | cytotoxic T's= effector cells helper T's (assist other cells) both are regulatory cells suppressor T's (turn down or depress activity) |
| CD4 CD8 | most helper T's (refer to specific glyoproteins) |
| what is dual "double" recognition? | When t-cells must recognize- 1) their specific antigen 2) correct cell surface proteins |
| when do T-cells recognize antigen and respond to it? | Only when presented or attached to our own body cells |
| what are the 2 steps in t-cell activation? | 1. antigen binding 2. co-stimulation |
| co-stimulation is? | -binding to additional receptors (on APC) ex. B, proteins -cytokines; chemicals from macrophages or other t-cells |
| Anergy | Just binding...skipping steps |
| what is cytokines? | it is chemicals from immune system cells |
| types of cytokines | -interferons -interleukin 1 (macrophages) -interleukin 2 (helper t's) -perforin=cytotoxic t's (main weapon -complement...and more |
| Cytotoxic T's | the effectors of the cell mediated response |
| -directly attack other cells -main targes are viruses-infected cells -recognize antigen with class I MHC proteins -release perforin=forms holes in target cell allowing CA++ to enter, killing cell -may also use other chemicals (lymphotoxic, etc) | Cytotoxic T's |
| Supressor T's (regulatory) | not as well known; thought to help "turn down" system when response is adequate |
| Helper T's (also regulatory) | play a central (pivotal) role in activation and function of all other immune system cells |
| autografts | from the same person |
| isografts | from a genetically identical person |
| allografts | from another, non-genetically identical person |
| xenografts | from a member of another species (baboon, pig) |
| why would cyclosporine or steroids be administered? | to suppress the immune system and inhibit rejection..they are anti-rejection drugs |
| Immunodeficeiencies | -SCID- born without ability to produce major immune system component acquired -Hodgkin's disease=cancer of the lymph nodes -AIDS= acquired immunodeficiency syndrome (targets helper T-cells |
| Autoimmune disorders | immune system goes haywire; loss of self/anti-self identification *more common in women* |
| some examples of autoimmune disorders would be: | Multiple Sclerosis Myasthenia Gravis:skeletal muscle and nerve communication Grave's Disease- thyroid (hyper) Type 1 diabetes-cells that secrete insulin Lupus glomerulonephritis- kidneys Rheumatoid arthritis |
| Hypersensitivities | immune response out of proportion to the threat (abnormally vigours response) |
| the 2 types of hypersensitivities are: | acute: allergen-quick, strong response (system wide e.g anaphylaxis :bee sting or peanuts delayed: happens 3-5 days after exposure |
| lyse | explode |
Created by:
dmlee91
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