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23 Cards in this Set

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How are B cells activated and cloned?
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
What is the basic AB structure?
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.
What are the hinge and stem regions of an AB?
hinge:
-midregion of the 2 H chains
-high flexibility: either Y or T shape

stem:
-parts of the H chain beyond hinge region
What are the differences between the variable region and constant regions of ABs?
variable
-different for each AB

constant:
-similar in AB of same class
-basis for AB grouping into IgG, IgA, IgM, IgD, IgE
What are the different AB classes structures?
IgE, IgD, and IgG have same Y shape and are monomers

IgA can be both monomer or dimer

IgM is huge, a pentamer
What are the roles of each of the ABs?
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)
What are the actions of AB?
Neutralizing AG

Immobilizing bacteria

Agglutinating and precipitating AG

activating complement

Attracting phagocytes
What are Monoclonal AB?
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
What is the first step in activation of the complement system?
Activation of C3 (C3 --> C3a, C3b)
What is the process of activated Complement system?
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
What do each Complement system do?
C5b - C9 --> membrane attack complex

C3a, C5a --> anaphylatoxins stimulate release of histamine

C5a --> leucocyte chemtactic factor

C3b --> opsonin
What is Immunological memory?
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
What is clonal selection theory?
-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
What is active immunity?
natural acquired:
-exposure to pathogens --> plasma cells, cytotoxic T, T & B memory

artificially acquired:
-immunogenetic AG during vaccination --> immune response, production of memory cells
What is passive immunity?
naturally acquired:
-transfer of antiobodies (ex. mother to fetus)

artificially acquired:
-intravenous injection of AB
What is self-recognition?
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
What is self-tolerance?
lack of reactivity to self peptide fragments

cells that recognize self-AG undergo apoptosis (deletion) or anergy (inactivation)
What is an Autoimmune disease?
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
What is an Immune Complex Disease?
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
What is allergy?
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
What happens in an Anaphylactic Reaction?
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
What are cytotoxic reactions?
caused by AB (IgG or IgM) against blood cells

activation of complement system

cell lysis (transfusion of incompatible blood)
What is delayed hypersensitivity?
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