03 B Cells
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BCR
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FAB: fragment antigen binding
FC: constant
Made of monomer IgM antibody
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purple: variable regions. Vary from 1 B cell to another
light chain: 1 constant region; heavy chain 3 constant regions
variable regions end in nitrogen groups; constant end in carboxyl group
Connected by disulfide bridges
macrophage Fc/protein A binds CH2-CH3 region
Heavy chain
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Activation
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B cell crosslinked by antigen
Second signal required in addition to crosslinking
MHC 2 binds TCR and CD4
CD40 binds CD40L: class switching
B7 binds CD28: T cytokine secretion
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macrophage antigen presenting instead
T Independent
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so many antigen on surface, B cell activated without T
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Conjugated Vaccine
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Surface Proteins
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CD21 receptor for complement, receptor for EBV
Antibody
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Protein A
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prevents opsonization:
Class Switching
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only change Fc portion, not FAB portion
Cm and Cd closes
Cm and Cd spliced out; B starts to make Cy (IgG), Ca, Ce
IgM
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Classical pathway: 2 C1 molecules bind together to Fc of IgM; easy to bind because so many IgM Fc together
Prevents attachment: very large and clumps on to pathogens
Weak opsonin: too big; macrophages can't get to Fc
IgG
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macrophages bind to Fc very easily
IgA
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secretory component in middle of 2 IgA
linked by secretory: can't complement
IgA Protease
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IgE
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Somatic Hypermutation
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Happens during proliferation after activation
Stronger binding will proliferate the most
B Cell Fate
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Development Timeline
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Vaccines
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active
passive
Active
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Live attenuated: T cell mediated response
Killed: antibodies against HA antigens of virus
Inactivated viral vaccines do not infect host cells and therefore do not enter the MHC class I antigen-processing pathway, which is normally required for the generation of a significant CD8+ cell-mediated immune response. In contrast, live-attenuated viral vaccines strongly stimulate the MHC class I antigen-processing pathway and can generate cytotoxic CD8+ T lymphocytes that kill infected cells.
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Passive
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give if suspicion for rabies, tetanus: neutralize before infection happens
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