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26 Cards in this Set
- Front
- Back
8.1
humoral immune response: |
- extracellular space protected by humoral immune response
- Abs produced by B cells cause destruction of external microorganisms and prevent spread of intracellular infections |
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8.2
B cell activation: |
- humoral immune response
- Ag bound by surface immunoglobulin (BCR) - internalize Ag -> degraded and processed - peptide fragment presented on the B-cell attached to its MHC II - armed helper T cells w/ TCR interacts w/ B cell -> signaling inside the Helper T cell - cytokines are released and completes the activation of B cell |
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8.3
Antibody secretion |
- humoral immune
- B cell activated to proliferate and differentiate into plasma (release Ab) and memory cell |
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8.4
Adhesins: |
- cell surface bacterial molecules
- bind to cellular receptors on target cell surface - endocytosis -> bacteria enters cell |
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8.5
toxins: |
- adhesins for viruses
- 2 components - 1 part bind a cellular receptor -> virus internalized - other part released ijnto cytoplasm to poison the cell |
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8.6
neutralization |
- 1 of the ways that antibodies prevent spread of infections
- antibodies prevent the pathogen and bacterial toxins from entering the cells by binding to adhesin molecules on their surface - IgA (mucosal surface) - IgG (within tissue) |
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8.7
complement activation |
- one of the ways that Ab prevent the spread of infections
- antibody activates complement proteins which enhaces opsonization and/or lyses bacteria by activating enzymes that create pores in their membrane |
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8.8
opsonization |
- a way that Ab prevent spread of infections
- alter the pathogen surface so it is targeted for ingestion by phagocytes - antibodies coat pathogen by binding their cell surface adhesins - Ab constant region recognized by Fc Receptors (FcR) on the surface of phagocytes (Macrophages) - Ab + FcR -> phagocytosis |
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8.9
virus-infected cells: |
- virus infected cells can communicate to the immune system by expressing viral molecules on their cell surface
- infected cell coated w/ antibody and recognized by FcRecptors (FcgammaRIII) on the surface of NK - NK release cytoplasmic granules containing perforin and other enzymes to desotry the whole cell |
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8.10
large parasites: |
- can't be ingested by phagocytes
- coated w/ IgE antibody - constant region of the antibody is bound w/ high affinity to FceReceptor I (FceRI) on the surface of eosinophils -> release toxic from inside the eosinophils onto the surface of the parasite |
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8.11
Ab-dependent cell-mediated cytotoxicity ADCC |
- destruction of target cells by NK cell
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8.12
Thymus-dependent antigen: |
- activation of B-cell with the presence of T cell
- 2 signals are required 1) signal from BCR 2) Signal from armed Helper T cell |
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8.13
Signal from armed Helper T cell |
- antigen is broken down and peptide is prosented on MHC II
- peptide is recognized by a helper T cell w/ TCR - signal transmitted inside the helper T -> induce CD40 -> interacts w/ B cell's CD 40 adhesion molecule -> helper T cell to produce and secrete cytokines into surrounding area - cytokines bind to a 2nd receptor on B -> B is activated |
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8.14
armed helper T cell |
- have been primed earlier in the infection by immune cells such as macrophages or dendritic cells
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8.15
thymus-independent antigens: |
- thymus independent (TI) antigens, can activate B cells w/o signal from helper I -> signal is from the antigen itself
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8.16
TI-1 antigens |
- induce B cell activation in mature and immature B cell
- high doses of antigen: polyclonal activation: nonspecific antibody resonse - low doses of antigen:L only interact with B cells that have specificity for the antigen: antigen specific resonse |
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8.17
TI-2 antigena |
- no intrinsic B cell stimulatory activity
- can only activate mature B - young children not good w/ this type of response |
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8.18
mature B cell: |
can produce antibodies in the periphery
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8.19
immature B cell |
still developing in bone marrow
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8.20
linked recognition: |
- before B cell activation CD4 + T (helper) cell must be activated by interaction w/ MHC/peptide on DC or macrophage or B itself
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8.21
how B cells grow up: |
- develop in bone marrow to mature
- mature B travel through periphery -> lymph node -> primary follicle (white region of lymph node) - some B activated here at B-T cell border - B-cell form primary foci in medullary cords (region below T cell zone), but they eventually form the Germinal center |
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8.22
Germinal Center: |
- if follicle contains a germinal center, it is no longer primary -> its now secondary follicle
- site where B proliferate and differentiates -> plasma and memory - plasma -> bone marrow -> antibodies |
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8.23
light zone (germinal center) |
- rapid B cell proliferation
- contain centrocytes |
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8.24
dark zone (germinal center) |
- intense proliferation
- somatic hypermutation |
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8.25
affinity maturation |
- selection of b cells that have high affinity for Ag binding and destruction of those that don't
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8.26
isotype switching |
- decline of IgM, rise in IgG
- IgM is the first that's produced |