z-logo
open-access-imgOpen Access
T FcγRIIIA‐158F allele is a risk factor for systemic lupus erythematosus
Author(s) -
Koene Harry R.,
Kleijer Marion,
Swaak Anton J. G.,
Sullivan Kathleen E.,
Bijl Marc,
Petri Michelle A.,
Kallenberg Cees G. M.,
Roos Dirk,
von dem Borne Albert E. G. K.,
de Haas Masja
Publication year - 1998
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199810)41:10<1813::aid-art13>3.0.co;2-6
Subject(s) - medicine , genotype , immunology , allele , lupus nephritis , lupus erythematosus , allele frequency , polymorphism (computer science) , population , antibody , biology , gene , genetics , disease , environmental health
Objective To study whether the FcγRIIIA‐158V/F polymorphism, which affects IgG binding affinity, is a risk factor for systemic lupus erythematosus (SLE). Methods We genotyped a group of 70 Caucasian SLE patients for all known FcγR polymorphisms. Of this group, 45 patients (64%) had nephritis. In 35 patients, this diagnosis was confirmed by renal biopsy. Results In the total group of 70 SLE patients, the frequency of the FcγRIIIA‐158F allele was 0.74, versus 0.57 in healthy controls ( P = 0.003). The genotype distribution of the FcγRIIIA‐158V/F polymorphism was also significantly different from that of the control population ( P = 0.004). The distribution of the other FcγR polymorphisms‐ FcγRIIA‐131R/H, FcγRIIIBNA(1,2) , and FcγRIIIA‐48L/R/H ‐was similar in SLE patients and controls. Conclusion In our group of SLE patients, only the distribution of the alleles of the FcγRIIIA‐158V/F polymorphism was significantly different from that in the control group. This might indicate that macrophage expression of the FcγRIIIA‐158F isoform is involved in the disturbed clearance of immune complexes in patients with SLE.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here