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23 Cards in this Set
- Front
- Back
How are B cells activated and cloned?
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activation:
-bind to BCRs -combined with MHC-II and moved to plasma membrane where helper T cell binds and delivers costimulation (IL-2) Clone: -plasma cells secrete AB -Memory cells wait for next time antigen comes -each cell in clone only secretes one type of AB ONLY B CELLS CAN RESPOND TO UNPROCESSED ANTIGEN |
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What is the basic AB structure?
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based on IgG
four polypeptide chains by disulfide bonds 2 Heavy, 2 Light Each chain has a Variable region (which is next to the hinge region) and a Constant Region Variable region is the antigen-binding site, each AB monomer has 2 antigen-binding sites. |
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What are the hinge and stem regions of an AB?
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hinge:
-midregion of the 2 H chains -high flexibility: either Y or T shape stem: -parts of the H chain beyond hinge region |
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What are the differences between the variable region and constant regions of ABs?
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variable
-different for each AB constant: -similar in AB of same class -basis for AB grouping into IgG, IgA, IgM, IgD, IgE |
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What are the different AB classes structures?
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IgE, IgD, and IgG have same Y shape and are monomers
IgA can be both monomer or dimer IgM is huge, a pentamer |
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What are the roles of each of the ABs?
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IgM - first antibody released to blood by plasma cells
IgG - most abundant antibody, crosses placental barrier. Accounts for passive immunity that a mother transfer to fetus. IgA - secretory, found in mucus. Found in women's breast milk IgD - always bound to a B cell surface, acts as a BCR IgE - involved in allergies and hypersensitivity reactions (basophils and mast cells) |
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What are the actions of AB?
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Neutralizing AG
Immobilizing bacteria Agglutinating and precipitating AG activating complement Attracting phagocytes |
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What are Monoclonal AB?
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fusing of tumor cells and B lymphocytes, called hybridomas
proliferate indefinitely (tumor) and produce a single AB (B) will be either IgG, IgA, or IgM used for sore throat and to measure drug level in blood |
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What is the first step in activation of the complement system?
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Activation of C3 (C3 --> C3a, C3b)
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What is the process of activated Complement system?
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Oposonization:
-phagocytes have receptors for C3b -C3b bind to binds to phagocyte and victim cell forming bridge between 2 C3a and C5a stimulate mast cells to secrete histamine: -increase blood floow and capillary permeability -increase emigration of phagocytes C5b and C6-C9 are inserted into bacterial cell membrane to form Membrane attack complex (MAC): creates large pores in membrane causing influx of H20 - cytolysis |
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What do each Complement system do?
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C5b - C9 --> membrane attack complex
C3a, C5a --> anaphylatoxins stimulate release of histamine C5a --> leucocyte chemtactic factor C3b --> opsonin |
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What is Immunological memory?
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primary immune response is first exposure to the antigen
response has 3 - 6 day lag period gives B cells time to proliferate and differentiate into plasma cells plasma antibody levels peak in 10 days then decline 2nd response is very fast this is called immunological memory |
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What is clonal selection theory?
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-B lymphocyte can produce AB
-T lymphocyte can respond to AG Exposure stimulates lymphocytes to dive many times until large population of clones is produce |
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What is active immunity?
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natural acquired:
-exposure to pathogens --> plasma cells, cytotoxic T, T & B memory artificially acquired: -immunogenetic AG during vaccination --> immune response, production of memory cells |
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What is passive immunity?
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naturally acquired:
-transfer of antiobodies (ex. mother to fetus) artificially acquired: -intravenous injection of AB |
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What is self-recognition?
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ability to recognize self MHC proteins
develops through positive selection of pre-T cells in thymus pre-T cells interact with self MHC proteins --> surviving of these T cells cells that don't interact --> apoptosis |
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What is self-tolerance?
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lack of reactivity to self peptide fragments
cells that recognize self-AG undergo apoptosis (deletion) or anergy (inactivation) |
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What is an Autoimmune disease?
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failure to recognize and tolerate self antigens
ex. -AB against thyroglobulin -Graves disease - auto AB mimics TSH -Myasthenia Gravis: auto AB block Ach receptors -Rheumatic fever: foreign antigens cross react with self antigens -Diabetes mellitus: cytotoxic T cells destroy self-cells |
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What is an Immune Complex Disease?
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damage produced by inflammatory response (AB-AG complex)
AG-AB complex is free rather than attached to bacteria leads to deposition of excessive AG-AB complexes in basement membrane activation of complement proteins and promotion of inflammation ex. rheumatoid arhtritis adn glomerulonephritis |
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What is allergy?
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immunological hypersensitivity to substances tolerated by most people
allergens - AG that induce allergic reactions types: antibody mediated: -Type I: anaphylactic immediate hypersensitivity -Type II: cytotoxic reactions -Type III: immuno-complex reactions cell mediated: -Type IV: delayed hypersensitivity |
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What happens in an Anaphylactic Reaction?
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occurs within few minutes once exposed to an allergen
exposure --> increase in IgE AB by B cells -attach to mast cells and basophils -stimulates secretion of histamine, leukotrienes, kinins, and prostaglandin D effects: -vasodilation -increase capillary permeability, increase fluid loss -lower BP -contraction of bronchial smooth muscles (difficulty breathing) 2nd time exposure will be fatal |
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What are cytotoxic reactions?
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caused by AB (IgG or IgM) against blood cells
activation of complement system cell lysis (transfusion of incompatible blood) |
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What is delayed hypersensitivity?
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12-72 hrs after exposure to AG
release of gamma interferon by T cells --> activates macrophages relase of TNF --> stimulates inflammation symptoms caused by secretion of lymphokines NOT histamine causes TB |