Term
| Describe the role of antigen receptors and co-receptors in B cell activation |
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Definition
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Term
| Describe differences between T independent and T dependent B cell responses |
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Definition
TI antigens: 2 types
-TI-1 stimulate R such as TLR
-TI-2 are repetitive epitopes that generally activate B-1 B cells
-Don't require T cells (athymic pts can respond)
-Predominately IgM (no isotype switching)
-Lack of somatic hypermutation
T dependent antigens:
-requires T cell help
-memory responses are generated
-isotype switching occurs
-somatic hypermutation: fine tuning Ab specificity |
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Term
| State the tissue location for T helper cell dependent B cell activation, and describe the cell interactions involved in this activation |
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Definition
Naive CD4 T cells are activated by antigens presented by dendritic cells in lymph node
Naive B cells activated by antigen are trapped in the *T-cell zone of the lymph node*
Antigen-activated B cells present antigen to helper T cells, forming cognate interactions and conjugate pairs
Second signal is provided to B cells by CD40/CD40L interactions and cytokines produced by T cells
-antigen binding to B-cell R delivers the first signal to B cell
-T cell recognizes antigen presented by MHC II by B cell --> conjugate pair (T cell and B cell)
-T helper cell delivers the second signal via CD40L and cytokines |
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Term
| Explain the development of high affinity B cell responses |
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Definition
-Activated B cell is bound to toxin, present peptide fragment to Th
-Cytokine and CD40L induce somatic hypermutation of B cell (Ig V regions) in rapidly proliferating germinal center centroblasts
-Some result in low-affinity centrocytes, B cell R is not cross-linked and centrocyte can't present antigen to T cell, dies
-Other option: germinal center centrocyte with high-affinity surface Ig results from somatic hypermutation
-binds antigen, gets activated, present it to T cell
-B-cell receptor is cross-linked, antigen is presented to Th
-centrocyte receives help, survives and divides |
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Term
Explain isotype switching and the _________ involved in this process
Hyper IgM syndrome |
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Definition
*Cytokines* induce isotype switching
Change from IgM to other isotypes - details not completely worked out
Hyper IgM syndrome results from a lack of CD40L - can't induce isotype switching
-produce very little IgG or IgA
-no germinal centers in lymph node
-no affinity maturation, b/c no somatic hypermutation |
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Term
| Describe the differences between resting B cells and plasma cells |
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Definition
Resting:
-expresses surface Ig
-expresses surface MHC class II
-doesn't make Ig
-undergoes growth, somatic hypermutation, isotype switching
Plasma:
-no expression of surface Ig (doesn't need to recognize antigen)
-no surface MHC class II (doesn't need to be activated by T cell)
-makes Ig!! (located in secondary lymphoid tissue, bone marrow)
-no growth, somatic hypermutation, isotype switching |
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Term
| List the major effector functions of antibody, including the primary antibody classes involved |
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Definition
Neutralization of viruses, bacteria, toxins
-IgA binds to virus, virus can't infect cells
-IgA Ab prevent attachment of bacteria to tissues; most bacteria are swept to gut, bacterial population is limited and kept at steady state
-Individuals w/o Ab get sick from infection
-Neutralizing Ab blocks binding of toxin to cell-surface R
Activate complement pathway (IgM)
-IgM effectively activates complement: once IgM binds to pathogen surface, it re-configures from planar form to "staple" form, can bind C1 -> activates classical pathway (classical C3 convertase)
-binding of 2+ IgG to a pathogen or soluble antigen can lead to complement activation
Opsonization (phagocytosis)
-Ab binds bacterium, Ab-coated pathogens are taken up by phagocytes
ADCC (Ab dependent cellular cytotoxicity)
-Ab binds antigens on target cell surface, NK Fc receptors recognize bound Ab, cross-linking of Fc R signals NK cell to kill target cell, target cell dies by apoptosis
Removal of immune complexes
Inhibition of immune responses
Induction of histamine and other inflammatory mediators
-IgE can induce allergies, but also protects against large parasites
-resting mast cell has preformed granules containing histamine and other inflammatory mediators; multivalent antigen cross-links IgE Ab bound at mast-cell surface -> release of granule contents
-IgE R are expressed by mast cells, basophils, eosinophils. Triggering of IgER --> degranulation --> contraction of smooth m in airways and gut, "forcing" large pathogens out of body |
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Term
| List the major pathway for complement activation that involves antibody |
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Definition
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Term
| List the distribution of the different isotypes of antibody |
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Definition
-IgM, IgG, IgA antibodies protect the blood, ECF, and internal organs
-IgG is the dominant isotype in the blood
-IgG is transferred from mother to fetus (passive immunity); it takes awhile for newborn to make its own IgG
-Dimeric IgA protects mucosal surfaces (nasal cavity, lungs, GI tract... helps protect against pathogens that enter these tracts)
-dimeric IgA is transferred from mother to baby in breast milk
-IgA and IgG are transported across epithelial barriers by specific receptor proteins
-FcRn helps transport IgG from blood to ECF
-poly-Ig R binds dimeric IgA, transports it from lamina propria to luminal surface
-IgE is primarily bound to IgE R on mast cells, basophils, activated eosinophils |
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