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Immune privilege in hair follicles

Jerry Shapiro, MD, University of British Columbia, Vancouver, BC

Alopecia areata and scarring alopecias are inflammatory hair loss diseases. Men, women, and children with alopecia areata or scarring alopecias develop large patches of hair loss caused by inflammatory cells disrupting hair growth. This event, particularly for women and children, can be psychologically devastating. The emotional distress often results in chronic depression and curtailment of social function. Research is required to understand these diseases and to find more effective treatments. Alopecia areata and scarring alopecias are believed to involve autoimmune mechanisms where the body’s own immune system mistakenly attacks a tissue or organ. One way that inflammatory hair loss disease may develop is if hair follicles fail to produce the correct chemical signals to protect them from inflammatory cells in the skin. If certain chemical signals are not produced by hair follicles, the immune cells may decide to attack the hair follicles resulting in alopecia areata or scarring alopecia. In this project, we will examine the hair follicle structure for the presence or absence of these protective chemical signals. We will identify the factors involved in providing hair follicle immune privilege and demonstrate how the factors might suppress immune cell activity by developing functional assays using cell culture methods. Potentially, if we identify one or more factors that provide immune privilege it may be possible to use these factors in the treatment of inflammatory hair loss conditions.

Peer reviewed publications supported by the Canadian Dermatology Foundation

1. Kang H, Wu WY, Lo BK, Yu M, Leung G, Shapiro J, McElwee KJ. Hair follicles from alopecia areata patients exhibit alterations in immune privilege-associated gene expression in advance of hair loss. J Invest Dermatol. 2010; 130: 2677-80.
2. Lo BK, Yu M, Zloty D, Cowan B, Shapiro J, McElwee KJ. CXCR3/Ligands are Significantly Involved in the Tumorigenesis of Basal Cell Carcinomas. Am J Pathol. 2010; 176: 2435-46.
3. Yu M, Bell RH, Ross EK, Lo BK, Isaac-Renton M, Martinka M, Haegert A, Shapiro J, McElwee KJ. Lichen planopilaris and pseudopelade of Brocq involve distinct disease associated gene expression patterns by microarray. J Dermatol Sci. 2010; 57: 27-36.
4. Zhang X, Yu M, Yu W, Weinberg J, Shapiro J, McElwee KJ. Development of Alopecia Areata Is Associated with Higher Central and Peripheral Hypothalamic-Pituitary-Adrenal Tone in the Skin Graft Induced C3H/HeJ Mouse Model. J Invest Dermatol. 2009; 129: 1527-38.
5. McElwee KJ. Etiology of cicatricial alopecias: a basic science point of view. Dermatol Ther. 2008; 21: 212-20.
6. Yu M, Zloty D, Cowan B, Shapiro J, Haegert A, Bell RH, Warshawski L, Carr N, McElwee KJ. Superficial, nodular, and morpheiform basal-cell carcinomas exhibit distinct gene expression profiles. J Invest Dermatol. 2008; 128: 1797-805.
7. Yu M, Kissling S, Freyschmidt-Paul P, Hoffmann R, Shapiro J, McElwee KJ. Interleukin-6 cytokine family member oncostatin M is a hair-follicle-expressed factor with hair growth inhibitory properties. Exp Dermatol. 2008; 17: 12-9.
8. Yu M, Finner A, Shapiro J, Lo B, Barekatain A, McElwee KJ. Hair follicles and their role in skin health. Exp Rev Dermatol. 2006; 1: 855-871.
9. Lu W, Shapiro J, Yu M, Barekatain A, Lo B, Finner A, McElwee KJ. Alopecia areata: pathogenesis and potential for therapy. Exp Rev Mol Med. 2006; 8: 1-19.