Alopecia areata: Hope for humans from helpful mice

27 August 2014 by Lowell Goldsmith - JID Jottings, posted in JID Jottings

Image of AA mouse model

AA mouse model

Cytotoxic T cells (CD8+NKG2D+) produce cytokines that interfere with human hair follicles, producing hair loss. Alopecia areata (AA) has been known in man for centuries. An appropriate and spontaneous natural mouse genetic model for AA was discovered a few decades ago in mice at Bar Harbor Laboratories in Maine, and it has been incredibly useful, as documented in several publications in the Journal of Investigative Dermatology and other journals. The mouse model is especially important as new therapies for this disease are contemplated. The cytotoxic T cells produce high levels of certain cytokines from JAK signaling. In the mouse model both systemic and topical JAK inhibitors, approved by the FDA for treating myelofibrosis, effectively inhibited AA and restored hair growth (Xing et al, 2014). In three humans with moderate to severe AA hair growth as "near complete" after 3-5 months of oral therapy with the JAK inhibitor ruxolitinib. This exciting beginning of a new therapeutic era will no doubt be followed by further studies of whether alopecia recurs when treatment is stopped, optimum treatment regimens, side effects, combined therapy with corticosteroids, and whether other JAK kinase inhibitors will work, etc.

This is a very important step for AA research and AA patients since this disease, which is often considered an orphan disease, should receive more attention from the pharmaceutical industry. Much of the basic and clinical research in AA which has allowed this progress has been supported by the NIH -- especially NIAMS, and the National Alopecia Areata Foundation. The editor is on an advisory board for the latter.

REFERENCE:

Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine advance online publication 17 Aug 2014 (doi:10.1038/nm.3645).

 

Image credit:  BMC Genetics 14:40, 2013; used with permission from Springer


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