Journal
HUMAN IMMUNOLOGY
Volume 73, Issue 4, Pages 421-425Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2012.01.013
Keywords
Chronic hepatitis B virus infection; CTLA-4; PDCD-1; Polymorphism; Interaction
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Funding
- National Natural Science Foundation of China [30972758]
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Programmed cell death 1 (PDCD-1) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) both negatively regulate the T-cell response in chronic hepatitis B virus (HBV) infection. This study determined genotypes of PDCD1 -606 G/A and +8669 G/A and CTLA4 -318 C/T and +49 A/G polymorphisms in 172 chronic HBV patients and 145 healthy controls and analyzed the interaction between these polymorphisms of the 2 genes. The results indicated that carriage of the PDCD1 +8669 A allele was increased in HBV patients carrying the CTLA4 -318 CC genotype and carrying the CTLA4 +49 AA genotype compared with controls carrying the CTLA4 -318 CC genotype (80.2% vs 64.8%, p = 0.002, odds ratio [OR] = 2.202, 95% confidence interval [95% CI] = 1.326-3.656) and carrying the CTLA4 +49 AA genotype (18.6% vs 9.7%, p = 0.024, OR = 2.139, 95% CI = 1.093-4.187), respectively. More obviously, carriage of the PDCD1 +8669 AA genotype was significantly increased in HBV patients carrying the CTLA4 +49 AA genotype compared with controls carrying the same CTLA4 +49 genotype (14.0% vs 3.4%, p = 0.001, OR = 4.541. 95% CI = 1.686-12.230). These results suggest that the PDCD1 +8669 A allele and AA genotype may amplify the predisposing effect conferred by the CTLA4 polymorphism through PDCD1 and CTLA4 gene interaction in chronic HBV infection. (C) 2012 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
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