Abstract
The contribution of individual Fcγ receptor (FcγR) subclasses to meningococcal phagocytosis was studied. In addition, functional FcγR polymorphisms were determined in 50 patients with meningococcal disease (MD), in 183 first-degree relatives of MD patients, and in 239 healthy control subjects, to study the association of FcγR genotypes with disease. Efficient internalization of opsonized Neisseria meningitidis serogroup B was mediated via multiple FcγR subclasses on phagocytes. Accordingly, a low-efficiency combination of Fcγ RIIa-R/R131, FcγRIIIa-F/F158, and FcγRIIIb-NA2/2 genotypes was increased significantly in relatives of patients with MD, compared with healthy control subjects (P < .05; odds ratio, 2.6; 95% confidence interval, 1.1-6.3). FcγRIIa and FcγRIIIa genotype distributions differed between patients with sepsis and those with meningitis. Combined genotypes of FcγRIIa and interleukin-10 -1082, which was previously reported as being associated with MD outcome, were distributed randomly in control subjects but not in relatives of patients with MD (P < 01). These data provide further evidence for the association of polymorphic genes on chromosome 1 and MD.
Original language | English |
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Pages (from-to) | 1548-1555 |
Number of pages | 8 |
Journal | Journal of Infectious Diseases |
Volume | 184 |
Issue number | 12 |
DOIs | |
Publication status | Published - 15 Dec 2001 |
Externally published | Yes |
Bibliographical note
Funding Information:Received 8 March 2001; revised 13 August 2001; electronically published 3 December 2001. Informed consent was obtained from patients and their relatives before study enrollment. Financial support: Netherlands Organisation for Scientific Research (NWO grant 95-10-624). a Present affiliation: Department of Neurology, University Medical Center, Utrecht, The Netherlands. Reprints or correspondence: Dr. W.-L. van der Pol, University Medical Center, Dept. of Immunology, Laboratory for Immunotherapy, KC.02-085.2, Lundlaan 6, 3584 EA Utrecht, The Netherlands ([email protected]).