03 B Cells
BCR
- FAB: fragment antigen binding
- FC: constant
- Made of monomer IgM antibody
- 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
Activation
- 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
- macrophage antigen presenting instead
T Independent
- so many antigen on surface, B cell activated without T
Conjugated Vaccine
Surface Proteins
- CD21 receptor for complement, receptor for EBV
Antibody
Protein A
Class Switching
- 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
- 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
- macrophages bind to Fc very easily
IgA
- secretory component in middle of 2 IgA
- linked by secretory: can't complement
IgA Protease
IgE
Somatic Hypermutation
- Happens during proliferation after activation
- Stronger binding will proliferate the most
B Cell Fate
Development Timeline
Vaccines
Active
- 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.
Passive
- give if suspicion for rabies, tetanus: neutralize before infection happens
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