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- Title
Genetic variants of the IgA Fc receptor (FcαR, CD89) promoter in chronic hepatitis C patients.
- Authors
Watanabe, Azuma; Shimokawa, Toshibumi; Moriyama, Mitsuhiko; Komine, Fumihiko; Amaki, Shuichi; Arakawa, Yasuyuki; Ra, Chisei
- Abstract
Fc receptor for IgA (FcαR, CD89) is capable of triggering IgA-mediated immune responses to pathogens and has been proposed to function in circulating IgA clearance. Because inheritable variations modifying individual immune responses or immunoglobulin catabolism may affect the chronicity of viral infection, we investigated whether promoter polymorphisms of the FcαR gene ( FCAR) affect chronic hepatitis C virus (HCV) infection and its disease progression. The two −311 T/ C and −142 T/ C single-nucleotide polymorphisms (SNPs) were studied by direct DNA sequencing in 177 Japanese patients with chronic hepatitis C (CHC). Both −311 CC and −142 CC genotypes were more frequent in CHC patients (15.9 and 18.6%) compared with 210 healthy controls (5.7 and 10.0%) [ p = 0.001, odds ratio (OR) = 3.10, 95% confidence interval CI) = 1.53–6.30 and p = 0.014, OR = 2.06, 95% CI = 1.14–3.72, respectively], and were associated with infection with HCV genotype 2a/2b ( p = 0.019 and p = 0.005, respectively). Conversely, −311 CC and −142 CC were decreased in 59 patients at advanced stages of disease as assessed on the basis of hepatic fibrosis markers such as decreased platelet count (PLT) ( < 150,000/μl) (5.1 and 8.5%) compared with 91 patients with normal PLT ( ≥ 150,000/μl) (24.2 and 26.4%) ( p = 0.006 and p = 0.005, respectively). Moreover, among the patients with normal PLT (but not with decreased PLT), −311 CC or −142 CC was significantly associated with decreased serum IgA levels ( p = 0.023 or p = 0.007, respectively). These results suggest that the FCAR promoter SNPs may be related to chronic HCV infection and disease progression in Japanese CHC, which might be explained by altered FcαR expression affecting IgA-mediated immune responses and/or IgA catabolism.
- Subjects
IMMUNOGLOBULIN A; HEPATITIS C; VIRAL hepatitis; BIOLOGICAL variation; IMMUNOGLOBULINS; VIRUS diseases
- Publication
Immunogenetics, 2006, Vol 58, Issue 12, p937
- ISSN
0093-7711
- Publication type
Article
- DOI
10.1007/s00251-006-0159-5