FIM2 Antibodies primarily target two distinct antigens:
Human CSF1R: A tyrosine-protein kinase receptor encoded by the CSF1R gene, involved in macrophage/monocyte regulation .
Bacterial Fimbrial Protein: A serotype-specific fimbrial subunit in B. pertussis (UniProt ID: P05788), critical for epithelial adhesion and immune evasion .
This article emphasizes the bacterial FIM2 due to its prominence in vaccine research and pertussis immunology.
FIM2 enables B. pertussis to:
Resist host clearance by adhering to respiratory epithelium .
Evade immune responses through antigenic variation (Fim2 vs. Fim3) .
Trigger antibody-mediated aggregation, enhancing bacterial clearance .
Key Mechanism: Anti-FIM2 antibodies induce bacterial aggregation and direct bactericidal effects, reducing NF-κB activation and pro-inflammatory cytokines in host cells .
DTaP5 (5-component acellular vaccine) elicits 3–6× higher anti-FIM2 responses than anti-FIM3 .
DTwP (whole-cell vaccine) produces more uniform but lower FIM2-specific responses .
Increasing FIM2/3 content in acellular pertussis (aP) vaccines improves efficacy:
Mouse Challenge Studies:
| Vaccine Formulation | Colonization Reduction | Efficacy Against FIM3 Strains |
|---|---|---|
| Standard aP | 40% | Moderate |
| High FIM2/3 aP | 75% | High |
Serotype Shifts: Post-vaccination serotype dominance (Fim2 → Fim3) correlates with reduced DTaP5 effectiveness over time .
Natural Infection: Anti-FIM2 IgG persists longer than anti-FIM3, suggesting FIM2’s superior immunogenicity .