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Don't kill pathogens but mark them so other cells kill them. Are effective against bacteria, viruses, toxins, and pathogens.Find an antigen that matches its receptor. It has to be activated by a T-Helper cell. The cell divides and produces a memory and plasma cell. |
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produce antibodies that attack the current type of antigen, other cells eat the cell that is marked by antibody and eat them. |
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effective against infected body cells, cancer cells, and foreign invaders. The directly attack cells or diseased host cells. |
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(Ag) something that causes you to make antibodies-Antigen generator. Each antigen contains many different epitopes, therefore there are many different anitbodies for each epitope. |
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the parts of a pathogenic cell where t-cell bind to with their specific receptor, each cell has a receptor that must bind to a specific site (epitope) |
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are inserted in lympocyte membranes before they leave the bone marrow and thymus. Each lympocyte displays only one type of antigen receptor and it also spends its whole life waiting for its epitope. |
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haptens/incomplete antigens |
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small molecules such as peptides or horomones that bind to body proteins, which produce immunogenicity. 1st exposure causes sensitization but 2nd causes a full blown immune response. |
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Major histocompatability complex-proteins are made inside the cell. Healthy cells make "normal" protein. Diseases make abnormal…etc |
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they take proteins from inside the cell and displays them on the cell surface |
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molecules that are found in every cell in the body. It is kind of like a meter indicating the balance of proteins within the cell. Tc cells react to MHC 1 when it displays diease or pathogen.\ |
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molecules that are only found in APCs. |
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include macrophages and dendritic cells and b cells. APC eat antigens then present their epitoes to lymphocytes. They also displaying MHC 2 on their shirts and T-lymphocytes see this so they attack. Apcs also display self antigens and t-cells ignore these but if they display an abnormal antigen then they will attack. Afer processing antigens the migrate to the LYMPH NODE. |
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Cytokines and Interleukins |
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cytokines-carries signal to other cells. Interleukins-cells participate in immune responses like inflammation. |
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T-cells general birth and training |
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Arise from lympocyte stem cell in RBM. Thymosins stimulate maturing cells to produce antigen receptors. Immunocompetent cells have receptors in place. Are tested in the thymus before they leave. |
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are immunocompetent cells that have not met the antigen they were programmed to find. They must be tested before they can go out. |
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Positive & negative selection |
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Immunocompetent cells must be able to recognize MHC protein by 1. responding to pop-up target. 2.Not react to pop-up target (if it is a good guy) |
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Clonal deletion and Anergy |
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If T-cells don’t pass the test they do not get cloned and are exicuted or they become inactive (alive but non-responsive). |
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Arise from lymphoid stem cell in RBM. Mature in RBM. These guys go through the same testing as t-cells. They create ANTIBODIES and mark for destruction but do not kill anyone. |
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Kill foreign cells and your own body's infected cells. |
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Assist in both processes. They are called cell mediated because they connect everything together.They attack foreign cells and diseased host cells & maintain memory of the antigen. |
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1.Tc-(CD8)cytotoxic-carry out attack 2. Th cells-(CD4) help promote Tc cells and B-cell action & non-specific defense mechanisms. 3. Tm cells-immune against exposure. 4. Tr cells-supressor cells that limit the immune response so our body doesn't over do the killing. |
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Cluster of differentation-is used to classify the cell surface markers in wbc. The Cd act as receptors or ligands. |
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Patrol the lymph nodes and respond to 2 types of MHC proteins. |
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recognize APC celss with MHC-2. They create clones that secret cytokines & interleukins. Attrack macrophages, NK ,neutrophils, & B-cells. They are the MOBILIZERS. And they co-stimulate T & B cell mitosis and maturation. |
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React-KILLERS- respond only to MHC-1 proteins and diseased cells. They release perforin and granzymes-(poke hole an kill cell with chemicals), interferons-(kill viruses and signal other cells etc), tumor factors-(Necrosis factor which kills cancer). |
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Exist in high #, follow clonal selection, some t- cells become memory t-cells, act quick to the same viruse, more memory cells that there are niave cells. |
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Recognize, React, Remember |
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Humoral Mechanisms RECOGNIZE |
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B-cell receptors bind antigen and takin in & digest antigen then display their epitopes on its MHC 2 protein. After activation by Th cell, they divide repeatly, differenciate into plasma cells, plasma cells produce antibodies for that particular pathogen for 4-5 days 2000 a second. |
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antibody bind to antigen reder it harmless don’t kill it but tag it so NK and Tc cells and other wbc can kill it. |
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Neutralization, complete fixation, aggultination, precipitation |
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Antibodies mask pathogenic region of antigen, make it helpless, attract Tc, NK, neutrophils, esoniophils, etc |
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Antigen binds to lgM or lgG, antibody changes shape, initiates complete binding, primary defense against foreign cells, bacteria |
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antibody binds antigen molecules (not host cells) creates antigen-antibody comples that precipitates, phagocytized by eosinophils. |
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Immunoglobulin-y globin. Glycoproteins, shaped like a Y or T, consist of 2 heavy & 2 light chains, have constant & variable regions, function as receptors on B-cells and also freely in body fluid, CAN ONLY BIND TO SPECIFIC ANTIGEN IT HAS BEEN DESIGNED TO RECOGNIZE. |
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bind antigens, unique for each b-cell or plasma cell, can bind antigens causing neutrolization, immmobilization, aggluination, and precipitaion. |
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recgnized by other mmune cells and molecures, Nk cells, complement proteins, eosinophils. Allow foreign cells & molecules to be targeted for destruction. |
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Immune system produces billion of diff Ab. Somatic recombination by DNA combination sequences that produces Ab genes, Somatic Hypermutation-B cells in lymph nodules rapidly mutate creating new sequences, can adapt to newly mutating Ag. |
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Pentamer-1st to respond during 1 degree immune response, Powerful aggultinator, complement fixation |
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dimer-found in body secretions (saliva, sweat , tears, milk, intestinal secrtetions) |
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monomer-b-cell membrane Ag receptor |
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monomer. 70-80% of circulatin antibodies, crosses placenta to feture, prominient in 2 degree immune response, complement fixation. |
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monomer-Toublemakers, om mast cells & basophils, stimulates release of histamine, attracks eosinophils, respond immediate hypersensitivity reactions. |
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Active immunity
Natural and artifical |
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In general it is when you make your own antibodies. Natural active immunity-naturally encounter the disease & your body makes Ab. Fake active immunity-when someone gives you a vaccine like the chicken pox, your body produces antibodies. |
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Passive Immunity
Natural and Fake |
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This is when you get someone else's antibodies. Natural-you get it from your mom (placenta & breast milk). Passive-someone injects antibodies in you |
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Hypersensitivity Reaction |
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Allergy- your body reacts to antigens excessively (that other people can usually tolerate) |
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In mast cells and basophils, Acute reactions like food etc. systemic-massive histamine release (people have to carry an epi pen) |
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delayed allergy, cosmetics, jewelry. |
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