B Cells- 5–10% circulating lymphocytes; arise from progenitor stem cell in bone marrow
- Express Ag-specific receptors on surface of cell; can present Ag to T cells but main function is development into plasma cells and produce Ab
- Primary immune response: naïve B cells encounter Ag → differentiate into memory cells or plasma cells; IgM produced initially but with help of T cells, B cells produce IgG, IgA, and IgE
- Secondary immune response: memory B and T helper cells re-exposed to Ag → memory B cells rapidly develop into plasma cells and release ↑↑ amount of Ab (faster, more efficient)
- Receptors/markers: MHC II molecules, complement receptors (recognize opsonized antigens), Fc receptors (immunoglobulin constant region), CD19, CD20, and CD79a
- Isotype switching occurs in presence of specific cytokines
| | | | | | | Table 1-11 Complement Fragments | | | Complement | | Function | | C3a | | Neutrophil chemoattractant | | C3b | | Potent agent of opsonization | | C3a, C4a | | Weak anaphylatoxins (promote inflammatory response by binding to complement receptor on mast cells and triggering release of histamine) | | C1 inhibitor | | Blocks spontaneous activation of C1 by plasma proteases | | C5a | | Most potent anaphylatoxin (neutrophil/mast cell degranulation, increased vascular permeability, chemoattraction) | | C5b | | Point of assembly for MAC formation | | | | | |
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| | | | | | | Table 1-12 Complement Deficiencies | | | Complement | | Function | | ↓ C1 inhibitor | | Hereditary angioedema (HAE); low levels in acquired angioedema as well | | ↓ C1–C4 (includes C1q, C1r, C1s) | | Increased risk of infections (especially encapsulated organisms like pneumococcus), SLE | | ↓ C3 | | Increased risk of infections, SLE, partial lipodystrophy, and glomerulonephritis | | ↓ C5–C9 | | Increased susceptibility to neisserial infections | | | | | |
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