Funding: Kyung Hee University Research Fund in 2008 (KHU-20081563).
Association between IL16 gene polymorphisms and susceptibility to alopecia areata in the Korean population
Article first published online: 10 DEC 2013
© 2013 The International Society of Dermatology
International Journal of Dermatology
Volume 53, Issue 3, pages 319–322, March 2014
How to Cite
Lew, B.-L., Chung, J.-H. and Sim, W.-Y. (2014), Association between IL16 gene polymorphisms and susceptibility to alopecia areata in the Korean population. International Journal of Dermatology, 53: 319–322. doi: 10.1111/ijd.12251
Conflicts of interest: None.
- Issue published online: 20 FEB 2014
- Article first published online: 10 DEC 2013
- Kyung Hee University Research Fund. Grant Number: KHU-20081563
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.
This study was conducted to determine whether variation in the IL16 gene contributes to risk for AA in the Korean population.
A total of 270 control subjects and 229 AA patients were enrolled. Genomic DNA was prepared from peripheral blood. Four single nucleotide polymorphisms (SNPs) (rs17875486 [promoter], rs17875491 [promoter], rs11073001 [exon], rs1803275 [exon]) of the IL16 gene were selected. Genotypes were determined by direct sequencing. Sequence data were analyzed. Multiple logistic regression models were calculated.
A significant difference emerged between the AA group and the control group for one SNP (rs17875491) of IL16. A further significant difference was found between patients with and without a family history of AA for a second SNP (rs11073001).
The present study found significant differences pertaining to two SNPs of the IL16 gene between, respectively, AA patients and controls (rs17875491) and AA patients with and without a family history of AA (rs11073001). Thus, IL16 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.