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Association between IL16 gene polymorphisms and susceptibility to alopecia areata in the K orean population
Author(s) -
Lew BarkLynn,
Chung JooHo,
Sim WooYoung
Publication year - 2014
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.12251
Subject(s) - alopecia areata , single nucleotide polymorphism , medicine , exon , genotype , snp , immunology , gene , genetics , microbiology and biotechnology , biology
Background Alopecia areata ( AA ) is a chronic disease that presents as non‐scarring hair loss. It is thought to be an organ‐specific autoimmune disease characterized by T cell infiltrates and cytokine production around anagen‐stage hair follicles. Interleukin‐16 ( IL ‐16) is a T cell‐specific chemoattractant known to be associated with autoimmune disease. Objectives This study was conducted to determine whether variation in the IL 16 gene contributes to risk for AA in the K orean population. Methods A total of 270 control subjects and 229 AA patients were enrolled. Genomic DNA was prepared from peripheral blood. Four single nucleotide polymorphisms ( SNP s) (rs17875486 [promoter], rs17875491 [promoter], rs11073001 [exon], rs1803275 [exon]) of the IL 16 gene were selected. Genotypes were determined by direct sequencing. Sequence data were analyzed. Multiple logistic regression models were calculated. Results A significant difference emerged between the AA group and the control group for one SNP (rs17875491) of IL 16 . A further significant difference was found between patients with and without a family history of AA for a second SNP (rs11073001). Conclusions The present study found significant differences pertaining to two SNP s of the IL 16 gene between, respectively, AA patients and controls (rs17875491) and AA patients with and without a family history of AA (rs11073001). Thus, IL 16 polymorphisms may play a role in the pathophysiology of AA or in the expression of AA phenotypes. Further studies are required to elucidate the role of IL ‐16 in the pathogenesis and clinical manifestation of AA .