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Original Article

PTPN22 1858C > T polymorphism and susceptibility to systemic lupus erythematosus: a meta-analysis update

, , , &
Pages 428-434 | Received 14 Feb 2017, Accepted 24 Sep 2017, Published online: 08 Oct 2017
 

Abstract

Studies performed in the past years showed PTNP22 1858 C > T (rs2476601) polymorphism as associated with systemic lupus erythematosus susceptibility, although conflicting findings are still found. In this context, a powerful statistical study, such as meta-analysis, is necessary to establish a consensus. The aim of this study was to evaluate association studies between the PTPN22 1858 C > T polymorphism and SLE by a meta-analysis update, including three recently published studies in the last three years. A total of 3868 SLE patients and 7458 healthy individuals were considered herein, enclosing 19 studies from Asian, American, European and Latin ethnic groups. Odds ratio (OR) was performed for allelic, dominant and recessive genetic models. Statistically significant association was found between the PTPN22 1858 C > T polymorphism and susceptibility to SLE in all inheritance models. Allelic genetic model data (OR = 1.54, 95% confidence interval (CI) = 1.38–1.72, p value=.000) shows that T allele confers increased SLE susceptibility. As well as recessive genetic model (OR = 2.04, 95% CI = 1.09–3.82, p value = .030) for T/T genotype. Instead, dominant genetic model shows that C/C genotype confers lower susceptibility for SLE development (OR = 0.62, 95% CI = 0.54–0.72, p value = .000). In addition, we provided an ethnicity-derived meta-analysis. The results showed association in Caucasian (OR = 1.47, p value = .000) and Latin (OR = 2.41, p value = .000) ethnic groups. However, rs2476601 polymorphism is not associated nor in Asian (OR= 1.31; p value = .54) and African (OR = 2.04; p value=.22) populations. In conclusion, present meta-analysis update confirms that T allele and T/T genotype in PTPN22 1858 C > T polymorphism confers SLE susceptibility, particular in Caucasian and Latin groups, suggesting PTPN22 1858 C > T as a potential genetic marker in SLE susceptibility.

Acknowledgements

All work performed in our research group in under financial support from the following Brazilian funding agencies: CAPES, CNPq and FACEPE.

Disclosure statement

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

This work was supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico, Coordenaçâo de Aperfeiçoamento de Pessoal de Nível Superior.

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