Fcγ Receptor IIa (CD32) Polymorphism in Fulminant Meningococcal Septic Shock in Children

• Published in: The Journal of infectious diseases Vol. 170; no. 4; pp. 848 - 853
• Main Authors: Bredius, Robbert G. M., Derkx, Bert H. F., Fijen, Cees A. P., de Wit, Ton P. M., Haas, Masja de, Weening, Ron S., van de Winkel, Jan G. J., Out, Theo A.
• Format: Journal Article
• Language: English
• Published: United States University of Chicago Press 01.10.1994
• Subjects: Adolescent; Antibodies; Bacteria; Child; Child, Preschool; European Continental Ancestry Group - genetics; Fc receptors; Female; Humans; Immunoglobulin G - blood; Immunoglobulin G - classification; Infant; Infections; Major Article; Male; Meningitis, Meningococcal - genetics; Meningitis, Meningococcal - immunology; Neisseria meningitidis - immunology; Neutrophils; Neutrophils - immunology; Phagocytosis; Polymorphism, Genetic; Predisposing factors; Receptors; Receptors, IgG - genetics; Reference Values; Retrospective Studies; Sepsis; Septic shock; Shock, Septic - genetics; Shock, Septic - immunology
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/170.4.848

Antibodies are essential in host defense against Neisseria meningitidis. Therefore, interactions among IgG and Fc receptors (FcγR) on phagocytes may be crucial. Genetic polymorphic forms of FcγRIIa (CD32) express different functional activities. In a retrospective study, FCγR polymorphisms were determined in 25 children who survived fulminant meningococcal septic shock: 11 had FcγRIIa-R/RHl, the poor IgG2-binding allotype, which is a significantly more frequent rate than found in a healthy white population (44% vs. 23%; P = .028; odds ratio = 2.67; 95% confidence interval, 1.09-6.53). The relevance of this finding was further supported by the fact that neutrophils with the Fe/RIIa-R/R131 allotype phagocytized N. meningitidis opsonized with polyclonal IgG2 antibodies less effectively than did Ila-H/HHl neutrophils. Our findings suggest an important role for anti-TV. meningitidis IgG2 and the FciRUa polymorphism in host defense against systemic meningococcal infections.