TNFAIP3 gene rs10499194, rs13207033 polymorphisms decrease the risk of rheumatoid arthritis.

Ming-Jie Wang,Hui Zhang,Hao-Yu Yang,Yuan-Yuan Mi,Rui-Ping Liu,Xindie Zhou

doi:10.18632/oncotarget.12638

Abstract

Accumulating evidences suggested that tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene rs10499194, rs13207033 polymorphisms may be associated with the risk of rheumatoid arthritis (RA). However, these studies yielded contradictory findings. To clarify convincing associations, we conducted a comprehensive meta-analysis by searching in PubMed, Embase, and the China Knowledge Resource Integrated Database. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by using fixed-effect or random-effect models. A total of 13 case-control studies for rs10499194 polymorphism and 6 studies for rs13207033 polymorphism were included. Our data indicated that TNFAIP3 gene rs10499194, rs13207033 polymorphisms were associated with the decreased risk of RA. Stratification analyses of ethnicity indicated rs10499194, rs13207033 polymorphisms decreased the risk of RA among Caucasian populations, but not among Asian populations. In conclusion, this meta-analysis indicates that TNFAIP3 gene rs10499194, rs13207033 polymorphisms decrease the risk of RA, especially among Caucasian populations.

Highlights

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, which is characterized by chronic destructive inflammation in synovial joints
This meta-analysis indicates that tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene rs10499194, rs13207033 polymorphisms decrease the risk of RA, especially among Caucasian populations
Our data indicated that rs10499194 polymorphism was significantly associated with a decreased risk of RA among Caucasian populations (TT vs. CT+CC: odds ratios (ORs), 0.79; 95% confidence intervals (CIs), 0.72–0.86, P < 0.001, Figure 4), but not among Asian and African-American populations

Summary

INTRODUCTION

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, which is characterized by chronic destructive inflammation in synovial joints. The etiology of RA is poorly understood, but it is believed that complex genetic and environmental factors play important roles in the pathogenesis of RA [1]. Human leukocyte antigen (HLA) alleles are well recognized to be implicated in the pathogenesis of RA [3]. Family studies indicated that HLA alleles contribute to about 30%. (TNFAIP3), a deubiquitinating protein, is reported to play a pivotal role in T cell activation and inflammatory signaling [5]. It can deregulate NF-κB-dependent gene expression via deubiquitinating specific NF-κB signaling molecules [6]

RESULTS

DISCUSSION

MATERIALS AND METHODS

Literature search and criteria of inclusion

CONFLICTS OF INTEREST