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

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...

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Published inPathology, 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
LanguageEnglish
Published Germany Elsevier GmbH 01.03.2015
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Abstract 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.
AbstractList 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.
OBJECTIVERheumatoid 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.METHODSFollowing 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.RESULTSA 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.CONCLUSIONOur overall analyses indicated that TLR4 Asp299Gly polymorphism might contribute to RA pathogenesis.
Author Tizaoui, Kalthoum
Hamzaoui, Agnès
Naouali, Abir
Kaabachi, Wajih
Hamzaoui, Kamel
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Issue 3
Keywords SNPs
TLR genes
TLR4 Asp299Gly
Rheumatoid arthritis
Meta-analysis
Language English
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Snippet Rheumatoid arthritis (RA) is thought to be triggered by various genetic and environmental factors. Few human epidemiologic studies demonstrated that single...
OBJECTIVERheumatoid arthritis (RA) is thought to be triggered by various genetic and environmental factors. Few human epidemiologic studies demonstrated that...
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SubjectTerms 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
Title Association of Toll like receptor Asp299Gly with rheumatoid arthritis risk: A systematic review of case–control studies and meta-analysis
URI https://dx.doi.org/10.1016/j.prp.2014.11.001
https://www.ncbi.nlm.nih.gov/pubmed/25499175
https://search.proquest.com/docview/1658416340
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