Association of Toll like receptor Asp299Gly with rheumatoid arthritis risk: A systematic review of case–control studies and meta-analysis

• Published in: Pathology, research and practice Vol. 211; no. 3; pp. 219 - 225
• Main Authors: Tizaoui, Kalthoum, Naouali, Abir, Kaabachi, Wajih, Hamzaoui, Agnès, Hamzaoui, Kamel
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.03.2015
• Subjects: Alleles; Arthritis, Rheumatoid - genetics; Genetic Association Studies; Genetic Predisposition to Disease; Genotype; Humans; Meta-analysis; Polymorphism, Single Nucleotide; Rheumatoid arthritis; SNPs; TLR genes; TLR4 Asp299Gly; Toll-Like Receptors - genetics; SNPs; TLR genes; TLR4 Asp299Gly; Rheumatoid arthritis; Meta-analysis
• ISSN: 0344-0338; 1618-0631
• DOI: 10.1016/j.prp.2014.11.001

Rheumatoid arthritis (RA) is thought to be triggered by various genetic and environmental factors. Few human epidemiologic studies demonstrated that single nucleotide polymorphisms (SNPs) in Toll-like receptor (TLR) genes are associated with RA. We aimed to evaluate the effects of TLR polymorphisms on the risk of RA pathogenesis by using a meta-analysis approach. Following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines, a systematic search and meta-analysis of the literature was conducted. We screened the medical literature based on keywords search in MEDLINE and EMBASE ‘Toll-like receptor’, ‘polymorphism’, and rheumatoid arthritis. Meta-analyses were performed under the random-effects model by using: (1) recessive, (2) homozygous, (3) dominant, (4) codominant and allele contrast models. A total of 3086 cases and 3756 controls in nine studies were included in the meta-analysis. Association between TLR4 Asp299Gly and RA risk was marginally significant [OR=0.856 (95% CI, 0.716–1.022); P=0.086] in the homozygous model. AA and GG homozygote genotypes tended to be significant protective factors against RA risk. Our overall analyses indicated that TLR4 Asp299Gly polymorphism might contribute to RA pathogenesis.