ArticleClinical and experimental immunology2000
The role of Fcgamma receptor polymorphisms and C3 in the immune defence against Neisseria meningitidis in complement-deficient individuals.
Article in Clinical and experimental immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 79 citations in OpenAlex.
- Genetic risk factors for infection in patients with early rheumatoid arthritis.Genes and immunity · 2004Trial
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Human genetics of meningococcal infections.Human genetics · 2020Review
- A Rare Mutation in SPLUNC1 Affects Bacterial Adherence and Invasion in Meningococcal Disease.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2020Article
- Complement and Bacterial Infections: From Molecular Mechanisms to Therapeutic Applications.Journal of innate immunity · 2018Review
- Meningococcal Vaccinations.Infectious diseases and therapy · 2016Review
- Defective functions of polymorphonuclear neutrophils in patients with common variable immunodeficiency.Immunologic research · 2014Article
- Functions of Antibodies.Microbiology spectrum · 2014Article
- Early cytokine release in response to live Borrelia burgdorferi Sensu Lato Spirochetes is largely complement independent.PloS one · 2014Article
- A case of meningococcal sepsis and meningitis with complement 7 deficiency in a military trainee.Infection & chemotherapy · 2013Article
- Glutamate utilization promotes meningococcal survival in vivo through avoidance of the neutrophil oxidative burst.Molecular microbiology · 2011Article
- Biology and pathogenesis of the evolutionarily successful, obligate human bacterium Neisseria meningitidis.Vaccine · 2009Review
- Prognostic value of phagocytic activity of neutrophils and monocytes in sepsis. Correlation to CD64 and CD14 antigen expression.Clinical and experimental immunology · 2008Article
- The involvement of Fc gamma receptor gene polymorphisms in Kawasaki disease.Clinical and experimental immunology · 2007Article
- Genetic analysis of HLA, NA and HPA typing in type 2 diabetes and ASO.International journal of immunogenetics · 2006Article
- Two novel mutations in the C7 gene in a Korean patient with complement C7 deficiency.Journal of Korean medical science · 2005Article
- Complement component C7 deficiency in a Spanish family.Clinical and experimental immunology · 2003Article
- Bench-to-bedside review: genetic influences on meningococcal disease.Critical care (London, England) · 2002Review
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individuals with either a late (C5-9) complement component deficiency (LCCD) or properdin deficiency are at increased risk to develop meningococcal disease, often due to serogroups W135 and Y. Anti-meningococcal defence in both LCCD persons and properdin-deficient individuals without bactericidal antibodies depends mainly on phagocytosis. Three types of opsonin receptors are involved in phagocytosis by polymorphonuclear cells (PMN). These represent the polymorphic FcgammaRIIa (CD32) and FcgammaRIIIb (CD16b) receptors, and the C3 receptor CR3 (CD11b/CD18). When the distribution of FcgammaRIIa and FcgammaRIIIb allotypes was assessed in 15 LCCD and in 15 properdin-deficient patients with/without previous meningococcal disease, we found the combination of FcgammaRIIa-R/R131 with FcgammaRIIIb-NA2/NA2 allotypes to be associated with previous meningococcal disease (odds ratio 13.9, Fisher's test P = 0.036). No such relation was observed in the properdin-deficient patients. The importance of FcgammaRIIa allotypes was also demonstrated using in vitro phagocytosis assays. PMN from FcgammaRIIa-R/R131 homozygous donors internalized IgG2 opsonized meningococci W135 significantly (P < 0.05) less than PMN from FcgammaRIIa-H/H131 donors. When properdin-deficient serum was tested, it was observed that reconstitution with properdin resulted in enhanced PMN phagocytosis of the W135 meningococci (P = 0.001). This enhanced phagocytosis was parallelled by an increase in C3 deposition onto the opsonized meningococci W135 (r = 0.6568, P = 0. 01). We conclude that the occurrence of meningococcal disease in LCCD patients is associated with certain FcgammaR allotypes. Properdin-deficient individuals are susceptible to meningococcal disease because of an insufficient C3 deposition on the surface of meningococci, resulting in insufficient phagocytosis.
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