4.6 Article

Involvement of the bulge region with decreased expression of hair follicle stem cell markers in senile female cases of alopecia areata

Journal

Publisher

WILEY-BLACKWELL
DOI: 10.1111/j.1468-3083.2010.03956.x

Keywords

alopecia areata; bulge; CD200; keratin15

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Funding

  1. Keio University School of Medicine
  2. Keio Medical Society

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Background Alopecia areata (AA) is a common hair loss disorder characterized by cellular autoimmune reaction predominantly involving the bulbar portion of anagen hair follicles. In most cases of AA, the bulge stem cell area remains intact. Recently, a couple of molecules, such as keratin15 (K15) and CD200, have been identified as biomarkers of human bulge cells. Of note, an immunosuppressive molecule, CD200 is speculated to provide an immune privilege for bulge stem cells. Objective To investigate expression levels of stem cell markers, especially CD200, in two senile female cases of AA with unusual lymphocytic cell infiltrates surrounding both the bulge and the bulbar regions. Then, compare them with those in common AA cases without the bulge involvement. Methods Transverse sections containing the bulge levels were prepared from unaffected and affected lesions, respectively, from each AA group and immunohistochemical investigation using anti-K15 and CD200 antibodies was performed. Importantly, an approach to detect CD200 in paraffin sections was newly developed. Immunoreactivities of individual antibodies were compared between corresponding lesions in each patient group. Results In unaffected bulge lesions, K15 immunoreactivity was not different between bulge-involving AA and common AA groups, whilst that of CD200 was decreased in the former group. Both K15 and CD200 immunoreactivities were decreased in affected bulge lesions of bulge-involving AA compared to the bulge of common AA cases. Conclusion Selective downregulation of CD200 in the bulge area could contribute to the collapse of immune privilege with resultant unusual bulge involvement in a subset of AA. Received: 3 September 2010; Accepted: 30 November 2010

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