Genome-wide association study in alopecia areata implicates both innate and adaptive immunity

Lynn Petukhova, Madeleine Duvic, Maria Hordinsky, David Norris, Vera Price, Yutaka Shimomura, Hyunmi Kim, Pallavi Singh, Annette Lee, Wei V. Chen, Katja C. Meyer, Ralf Paus, Colin A. B. Jahoda, Christopher I. Amos, Peter K. Gregersen and Angela M. Christiano ()
Additional contact information
Lynn Petukhova: Columbia University, New York, New York 10032, USA
Madeleine Duvic: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Maria Hordinsky: University of Minnesota, Minneapolis, Minnesota 55455, USA
David Norris: University of Colorado, Denver, Colorado 80010, USA
Vera Price: UCSF, San Francisco, California 94115, USA
Yutaka Shimomura: Columbia University, New York, New York 10032, USA
Hyunmi Kim: Columbia University, New York, New York 10032, USA
Pallavi Singh: Columbia University, New York, New York 10032, USA
Annette Lee: The Feinstein Institute for Medical Research, North Shore LIJHS, Manhasset, New York 11030, USA
Wei V. Chen: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Katja C. Meyer: University of Lübeck
Ralf Paus: University of Lübeck
Colin A. B. Jahoda: University of Durham
Christopher I. Amos: M. D. Anderson Cancer Center, Houston, Texas 77030, USA
Peter K. Gregersen: The Feinstein Institute for Medical Research, North Shore LIJHS, Manhasset, New York 11030, USA
Angela M. Christiano: Columbia University, New York, New York 10032, USA

Nature, 2010, vol. 466, issue 7302, 113-117

Abstract: Alopecia areata genetics The genetic basis of alopecia areata, a common autoimmune disease that causes disfiguring hair loss due to the collapse of immune privilege of the hair follicle, is largely unknown. A genome-wide association study has now identified several susceptibility loci for alopecia areata, most of them clustered into eight genomic regions. The spectrum of gene activities affected implies the involvement of both acquired and innate immunity in the condition. Among significant associations are the ULBP genes that encode activating ligands for the natural killer cell receptor NKG2D, which have not been previously linked to autoimmune disease.

Date: 2010
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DOI: 10.1038/nature09114

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