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Partial restoration of hair growth in the DEBR model for alopecia areata after in vivo depletion of CD4+ T cells
Author(s) -
Kevin J. McElwee,
Elizabeth M. Spiers,
R. F. Oliver
Publication year - 1999
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1999.02705.x
Subject(s) - alopecia areata , in vivo , cd8 , hair loss , population , endocrinology , intraperitoneal injection , t lymphocyte , medicine , flow cytometry , cell growth , hair follicle , pathogenesis , immunology , biology , andrology , immune system , dermatology , biochemistry , microbiology and biotechnology , environmental health
Alopecia areata (AA) is widely believed to be an autoimmune disease. Hair loss is associated with a peri‐ and intrafollicular inflammatory infiltrate of anagen hair follicles primarily composed of CD4 + and CD8 + cells. A previous investigation involved in vivo depletion of CD8 + cells in the DEBR rat model to examine the cells' potential pathogenic activity in AA. The rat model is used here in a comparable study of CD4 + cell pathogenic activity. Eight AA affected DEBR rats were given intraperitoneal injections of a CD4 + cell depleting OX‐35/OX‐38 monoclonal antibody (MoAb) cocktail over a 15‐day therapy course. A further eight AA‐affected rats comprised a control group and were injected with equivalent volumes of an irrelevant MoAb, OX‐21. Changes in both CD4 + and CD8 + peripheral blood cell populations were analysed by flow cytometry, and macrophotography was used to record any changes in hair growth. Of the eight CD4 + cell‐depleted rats six responded with hair growth. The rats revealed significant hair growth within 23 days of treatment initiation. With rapid replacement of the CD4 + cell population the newly generated pelage hair was eventually lost. Two control rats also showed limited hair growth within the 112‐day study period. In vivo depletion of CD4 + cells partially restores hair growth in AA affected rats. The response suggests that CD4 + cells may be actively involved in the pathogenesis of AA. Further research may elucidate whether CD4 + cells have a direct effect on hair follicles or exert their influence through their classic T helper cell supporting role for CD8 + cells.