B Cell Immunity Flashcards

1
Q

T-independent B cell activation

A

thymus-independent antigens on bacteria are typically polysaccharides in repeating subunits, which sends a strong signal to B cells to start secreting antibodies (without the need for T cell activation)
*the Lipid A on the bacteria is involved in TLR 4 signaling

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2
Q

why is T-independent B cell activation suboptimal

A

-doesn’t induce somatic hypermutation/affinity maturation of the B cell
-don’t get a lot of class switching
-don’t get a lot of memory B cells or plasma cells

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3
Q

thymus-dependent antigens

A

antigens with a PEPTIDE component can be presented to T cells
-can lead to class switching and immunologic memory
-primary way that B cells are activated

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4
Q

T-dependent B cell activation

A
  1. Th cells are activated
  2. B-cell receptor mediated endocytosis; foreign antigen presented on MHC II and recognized by TCR
  3. CD40 receptor on B-cell binds CD40L on Th cell
  4. Th cell secretes cytokines (diff cytokines for Th1 vs. Th2) that determine Ig class switching of V cells; B cells are activated, undergo class switching and affinity maturation, and begin producing antibodies
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5
Q

linked recognition

A

if the T cell - B cell interaction is to occur, BOTH cells must recognize EPITOPES on the SAME protein or protein conjugate or bacteria/virus
*used for conjugate vaccines

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6
Q

how does a conjugate vaccine work

A

conjugate an epitope of the desired antigen to the tetanus toxoid protein (which we already recognize because most people have already had the tetanus toxoid vaccine)

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7
Q

why does linked recognition protect against autoimmunity

A

low probability that self-reactive T AND B cells for the SAME antigen will survive development

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8
Q

what do B cells require to undergo somatic hypermutation and affinity maturation

A

require T cell interaction

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9
Q

what is affinity maturation

A

cells that make mutations that increase affinity for the antigen have a stronger T-cell interaction and have a stronger stimulus to develop further

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10
Q

where do B cells develop

A

develop in the bone marrow; migrate to the spleen and lymph nodes; once B cells encounter antigen, they form a germinal center

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11
Q

three fates of activated B cells

A

after undergoing maturation, the B cells can:
1) undergo apoptosis
2) become a plasma cell and start pumping out antibodies
3) become memory B cells

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12
Q

where do plasma cells reside once formed

A

may remain in the medullary cords
-may migrate to other sites such as bone marrow and spleen

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13
Q

where do memory B cells go once formed

A

found at several sites, but particularly the BONE MARROW

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14
Q

what is the immunoglobulin that can transport across the placenta

A

IgG

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15
Q

what do different Fc receptors do

A

different Fc receptors on OTHER CELLS allow ANTIBODIES to have different biological functions

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16
Q

Fc receptor: CD64 (FcgammaRI)

A

-binds IgG
-cell types: macrophages, neutrophils, eosinophils, dendritic cells
-effect: ACTIVATION OF RESPIRATORY BURST; induction of killing; stimulation of uptake

17
Q

Fc receptor: CD16 (FcgammaRIII)

A

-binds IgG
-cell types: NK cells, eosinophils, macrophages, neutrophils, mast cells
-effect: INDUCTION OF KILLING (NK cells)

18
Q

Fc receptor: FcepsilonRI

A

-binds IgE
-cells: MAST CELLS, eosinophils, basophils
-effect: SECRETION OF GRANULES

19
Q

type I hypersensitivity reactions

A

cross-linking of IgE-Fc receptors mediates degranulation of mast cell, causing extensive release of granules

20
Q

how do antibodies and complement synergize

A

-complement and IgG antibody coat bacterium
-when C3b binds, bacteria are phagocytosed
-increases killing of the bacterium

21
Q

overview - how do cytokines drive class switching

A

cytokines from T cells drive new transcription and recombination in B cells to generate class switching

22
Q

where does class switching occur

A

in the GERMINAL CENTERS of the lymph nodes or spleen
*occurs prior to somatic hypermutation

23
Q

what immunoglobulin isotype does IL-4 induce

A

IgE (and IgG)