Strong direct and indirect evidence supports an autoimmune etiology for alopecia areata. T lymphocytes that have been shown to be oligoclonal and autoreactive are predominantly present in the peribulbar inflammatory infiltrate. Alopecia areata frequently occurs in association with other autoimmune diseases, such as thyroiditis and vitiligo, and autoantibodies to follicular components have been detected. Finally, the use of immune modulating drugs, including corticosteroids and contact sensitizers such as dyphencyprone, can be beneficial in the management of this disease. Recent studies have demonstrated that alopecia areata scalp skin grafted onto nude mice with severe combined immunodeficiency grow hair and that infiltrating lymphocytes in the graft are lost. It is now also possible to induce alopecia areata in human scalp explants on these mice by injecting T lymphocytes with scalp homogenate. Neuropeptides produced by cutaneous nerves are known to modify immune reactivity and, in all likelihood, affect the alopecia areata process. Future studies may show that modulation of neuropeptide expression is associated with hair regrowth. Likewise, testing the efficacy of the newly developed immunomodulatory agents in patients with alopecia areata may lead to the introduction of novel therapies for this immune-mediated disease of the hair follicle.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Investigative Dermatology Symposium Proceedings|
|State||Published - Jan 2004|
Bibliographical noteFunding Information:
The opportunity to establish a Registry for AA became a reality with grant support from the National Institutes of Health and the National Institute of Arthritis, Metabolism, and Skin Diseases. The goal of the protocol is to develop a registry from which subsequent analyses and selective patient sampling can be conducted. One goal is to search for associations between specific genetic markers, such as HLA-linked loci, and the development of AA. The overall goals are to understand the genetic control of autoimmunity in AA, to better understand the complex biology of the cycling hair follicle, and to use this knowledge to devise safe and effective treatments (Protocol Laboratory-0391). The operation of the registry is outlined in Figure 5 .
We thank Christine Baker for her assistance with the preparation of this manuscript. This work was supported in part by grants from the National Alopecia Areata Foundation and 3M Pharmaceuticals.
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