The hair follicle is described as an immune-privileged site, meaning hair growth is recognized as normal by the immune system (1,2). Strategies such as the use of “no danger signals” communicate that the hair follicle should be left exempt from an immune attack (3,4). Unfortunately, these signals can be shut down, leading to a collapse of immune-privilege, followed by an inflammatory response. Chronic hair follicle inflammation can then lead to the condition alopecia areata, which affects approximately 2% of the population (5).
Alopecia areata presents as a patchy hair loss on the scalp. In some cases, complete hair loss throughout the entire scalp occurs and is referred to as alopecia totalis. Alopecia universalis is hair loss over the full body including eyebrows and eyelashes. Fortunately, the immune-privilege can resolve itself, resulting in frequent spontaneous remissions.
So how is the immune privilege lost? Studies have suggested that collapse can be triggered by viral infections, trauma, hormones or stress (6,7). It could also be a matter of genetics with increased risk factors for those with affected first-degree relatives and those already diagnosed with a related autoimmune disease (6,8–12).
How can alopecia areata be treated? Officially there are currently no FDA approved therapies however there are several options which have had some success as well as new treatments recently entering the market. Steroids are often used as a first line of defense while topical sensitizers are employed in more severe cases or for those who suffer from chronic relapsing. Some of the most recent therapies include treatment with platelet-rich plasma as well as drugs designed to target the immune system specifically.
Speak with your hair-care specialist to learn more about which options would work best for you in addition to more information on the benefits and potential side effects of treatment.
Article by: Dr. J.L. Carviel, Mediprobe Research Inc.
References
- Ito T, Meyer KC, Ito N, Paus R. Immune privilege and the skin. Curr Dir Autoimmun. 2008;10:27–52.
- Paus R, Nickoloff BJ, Ito T. A “hairy” privilege. Trends Immunol. 2005 Jan;26(1):32–40.
- Rosenblum MD, Olasz EB, Yancey KB, Woodliff JE, Lazarova Z, Gerber KA, et al. Expression of CD200 on epithelial cells of the murine hair follicle: a role in tissue-specific immune tolerance? J Invest Dermatol. 2004 Nov;123(5):880–7.
- Rosenblum MD, Yancey KB, Olasz EB, Truitt RL. CD200, a “no danger” signal for hair follicles. J Dermatol Sci. 2006 Mar;41(3):165–74.
- Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl J Med. 2012 Apr 19;366(16):1515–25.
- McElwee KJ, Gilhar A, Tobin DJ, Ramot Y, Sundberg JP, Nakamura M, et al. What causes alopecia areata? Exp Dermatol. 2013 Sep;22(9):609–26.
- Peters EMJ, Liotiri S, Bodó E, Hagen E, Bíró T, Arck PC, et al. Probing the effects of stress mediators on the human hair follicle: substance P holds central position. Am J Pathol. 2007 Dec;171(6):1872–86.
- Van der Steen P, Traupe H, Happle R, Boezeman J, Sträter R, Hamm H. The genetic risk for alopecia areata in first degree relatives of severely affected patients. An estimate. Acta Derm Venereol. 1992 Sep;72(5):373–5.
- McDonagh AJG, Tazi-Ahnini R. Epidemiology and genetics of alopecia areata. Clin Exp Dermatol. 2002 Jul;27(5):405–9.
- Biran R, Zlotogorski A, Ramot Y. The genetics of alopecia areata: New approaches, new findings, new treatments. J Dermatol Sci. 2015 Apr;78(1):11–20.
- Barahmani N, Schabath MB, Duvic M, National Alopecia Areata Registry. History of atopy or autoimmunity increases risk of alopecia areata. J Am Acad Dermatol. 2009 Oct;61(4):581–91.
- Huang KP, Mullangi S, Guo Y, Qureshi AA. Autoimmune, atopic, and mental health comorbid conditions associated with alopecia areata in the United States. JAMA Dermatol. 2013 Jul;149(7):789–94.
