opsonization

Opsonization involves coating of antigens/pathogens with opsonins—primarily IgG (via Fc receptors, FcγR) and complement protein C3b/iC3b (via complement receptors, CR1)—which act as a molecular 'bridge' to enhance phagocyte binding and engulfment. This process is critical for the clearance of encapsulated bacteria (e.g., Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis), which have polysaccharide capsules that resist phagocytosis unless opsonized. Clinical relevance: Patients with complement deficiencies (e.g., C3 deficiency) or splenic dysfunction (asplenia, sickle cell disease) have impaired opsonization and are highly susceptible to infections with encapsulated organisms. Antibody deficiencies (e.g., X-linked agammaglobulinemia, CVID) also impair opsonization since IgG is a major opsonin. The spleen plays a key role by housing macrophages that clear opsonized bacteria from the blood. Vaccines against encapsulated bacteria (pneumococcal, meningococcal, Hib) work partly by generating opsonizing antibodies. This concept is tested frequently in the context of immunodeficiencies, splenectomy patients requiring vaccination, and complement pathway disorders.