TY - JOUR
T1 - The FcγRIIIA-158F allele is a risk factor for systemic lupus erythematosus
AU - Koene, Harry R.
AU - Kleijer, Marion
AU - Swaak, Anton J.G.
AU - Sullivan, Kathleen E.
AU - Bijl, Marc
AU - Petri, Michelle A.
AU - Kallenberg, Cees G.M.
AU - Roos, Dirk
AU - Von Dem Borne, Albert E.G.K.
AU - De Haas, Masja
N1 - Copyright:
Copyright 2004 Elsevier Science B.V., Amsterdam. All rights reserved.
PY - 1998/10
Y1 - 1998/10
N2 - 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, FcγRIIIB- NA(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.
AB - 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, FcγRIIIB- NA(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.
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U2 - 10.1002/1529-0131(199810)41:10<1813::AID-ART13>3.0.CO;2-6
DO - 10.1002/1529-0131(199810)41:10<1813::AID-ART13>3.0.CO;2-6
M3 - Article
C2 - 9778222
AN - SCOPUS:0031595344
VL - 41
SP - 1813
EP - 1818
JO - Arthritis and Rheumatology
JF - Arthritis and Rheumatology
SN - 2326-5191
IS - 10
ER -