Antibodies

Antibodies
Type Response Action
G Main Ab in 2° Complement activation,
response crosses placenta, opsonize
bacteria, neutralize toxins
and viruses
A Mucous membranes Prevent attachment of
microbes to mucous memb.
Does not fix complement
Neonatal passive immunity
M 1° response Complement activation, Ag
receptor on naïve B-cell
E Immediate Induces release of mediators
from mast cells and
basophils
Activate eosinophils
D Unclear
Other Hypersensitivity type
Most numerous II (cytotoxic) and III
Longest half-life (T1/2~month) (immune complex)
FcγRIII on NK cells for ADCC
Monomer or dimmer
In secretions (picks up secretory
component from epithelium)
T1/2~week
Does Not cross placenta
Monomer on B-cell or pentamer
Lowest concentration I (immediate) – allergy
Shortest T1/2
Immunity to worms
FcεRI on eosinophils for ADCC
On surface of naïve B cells

Isotype Switching
Default  IgM/D
- Helper T cells : CD40L, Cytokines switch
• IFN-γ  IgG
• IL-4  IgE
• TGF-β or mucosal tissue  IgA

Thymus Independent Ag
- Polymeric Ag (polysaccharides) – Not presented to B cells - Only IgM secreted
- Little isotype switching (maybe to IgG), basically ø memory

Ab Effector Fxns
- Neutralize microbes and toxins
- Opsonization and ↑ phagocytosis of microbes (requires x-linking as safety measure)
- ADCC (Ab Dependent Cellular Cytotoxicity)
- Complement Activation (3 pathways) (3 results)
• Alternative – C3
C3C3b + BbC3bBb(C3-convertase) + C3bC3bBb3b (C5-convertase)
• Classical – C1
IgG/M + C1 + C4b2b (C3-convertase) +C3bC4b2b3b (C5-convertase)
C4 + C2C4b +C2b ^
• Lectin – MBL
MBLC4b + C2bC4b2b +C3bC4b2b3b (C5-convertase)
• Once C3-convertase is attaced, C3 cleavage yields C3b which attaches to C3
convertase to form C5-convertase and covalently binds to the microbe (C3 opsonizes)
• C5-convertase cleaves C5C5b
• C5b binds C6,7, 8 and poly C9 sequentiallyMAC (Membrane Attack Complex)
which causes cell lysis
• C3b also cleaves C3,4,5C3a, C4a, C5a for inflammatory pathway (activate
leukocytes – ↑ cytokines and ROI)
• Host Cell has DAF, CR1 to displace Bb from C3b or MCP, CR1 as cofactor for Factor
1 to cleave C3b to make inactive, C1 INH prevents C1 from being active and cleaving
 Antibodies
C2 and C4 (stop complement cascade on healthy cells)