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CTLA4 +49AG (rs231775) and CT60 (rs3087243) gene variants are not associated with alopecia areata in a Mexican population from Monterrey Mexico How to cite this article: Salinas-Santander MA, Cantu-Salinas CS, Ocampo-Candiani J, Suarez-Valencia VJ, Ramirez-Guerrero JG, Sanchez-Dominguez CN. CTLA4 +49AG (rs231775) and CT60 (rs3087243) gene variants are not associated with alopecia areata in a Mexican population from Monterrey Mexico. An Bras Dermatol. 2020;95:283-8. ,☆☆ ☆☆ Study conducted at the Department of Investigation, Facultad de Medicina Unidad Saltillo, Universidad Autónoma de Coahuila, Coahuila, México, and Dermatology Service, Hospital Universitario Dr. José Eleuterio González, Facultad de Medicina, Universidad Autónoma de Nuevo León, Nuevo León, México.

Abstract

Background:

Alopecia areata is an autoimmune disease that produces non-scarring hair loss around the body. Gene variants of the cytotoxic T-lymphocyte antigen 4 (CTLA4) gene, a negative regulator of T-cell response, have been associated with a predisposition to autoimmune diseases in different populations; however, the involvement of these genetic variants in the development of AA is controversial.

Objective:

The present study evaluated the potential association of two CTLA4 gene variants with alopecia areata in a Mexican population.

Methods:

We genotyped +49AG (rs231775) and CT60 (rs3087243) variants in 50 AA patients and 100 healthy control participants through PCR-RFLP.

Results:

No statistical difference was observed for either of the gene variants regarding allele or genotype frequencies between AA patients and the controls when the parameters of family/personal history of autoimmune diseases or gender were considered (p > 0.05). Study limitations: Small sample size of patients and the data were obtained from Northeast Mexico population.

Conclusion:

The genetic variants rs231775 and rs3087243 of the CTLA4 gene are not a risk factor for the development of alopecia areata in the analyzed Mexican population.

KEYWORDS
Alopecia areata; Autoimmune diseases; Polymorphism; Single nucleotide

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