Editors' ChoiceAutoimmune Disease

"Dangerous" Hair

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Science Signaling  06 Jul 2010:
Vol. 3, Issue 129, pp. ec206
DOI: 10.1126/scisignal.3129ec206

Alopecia areata, which causes disfiguring hair loss, arises from autoimmune attack of the hair follicle. Petukhova et al. performed a genome-wide association study with data from more than 1000 alopecia areata patients (and >3000 controls) and found 139 single-nucleotide polymorphisms (SNPs). The regions containing the SNPs included genes that control the activation and proliferation of regulatory T cells, cytotoxic T cells, and TH17 T helper cells, suggesting that these may be targets for future study. Additionally, they found SNPs in the region containing the ULBP gene cluster, which encode cytomegalovirus UL16-binding proteins that serve as stress-induced “danger” signals and are activating ligands of the natural killer cell receptor NKG2D. Immunohistochemistry revealed that the abundance of ULBP3 in hair follicles from affected areas of scalp from patients with alopecia areata was increased in the dermal sheath and dermal papilla compared with the abundance in follicles of scalp samples from unaffected individuals. Furthermore, the affected scalp samples were infiltrated with cytotoxic T cells that were positive for NKG2D. Thus, it appears that aberrant production of a danger signal may contribute to this autoimmune disease.

L. Petukhova, M. Duvic, M. Hordinsky, D. Norris, V. Price, Y. Shimomura, H. Kim, P. Singh, A. Lee, W. V. Chen, K. C. Meyer, R. Paus, C. A. B. Jahoda, C. I. Amos, P. K. Gregersen, A. M. Christiano, Genome-wide association study in alopecia areata implicates both innate and adaptive immunity. Nature 466, 113–117 (2010). [PubMed]

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