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Maternal IL ‐6 can cause T‐cell‐mediated juvenile alopecia by non‐scarring follicular dystrophy in mice
Author(s) -
Smith Stephen E. P.,
Maus Rachel L. G.,
Davis Tessa R.,
Sundberg John P.,
Gil Diana,
Schrum Adam G.
Publication year - 2016
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12914
Subject(s) - alopecia areata , hair loss , hair cycle , alopecia universalis , hair follicle , scarring alopecia , biology , immunology , endocrinology , medicine , scalp , dermatology , genetics
Aiming to decipher immunological mechanisms of the autoimmune disorder alopecia areata ( AA ), we hypothesized that interleukin‐6 ( IL ‐6) might be associated with juvenile‐onset AA , for which there is currently no experimental model. Upon intramuscular transgenesis to overexpress IL ‐6 in pregnant female C57 BL /6 (B6) mice, we found that the offspring displayed an initial normal and complete juvenile hair growth cycle, but developed alopecia around postnatal day 18. This alopecia was patchy and reversible (non‐scarring) and was associated with upregulation of Ulbp1 expression, the only mouse homolog of the human AA ‐associated ULBP 3 gene. Alopecia was also associated with inflammatory infiltration of hair follicles by lymphocytes, including alpha‐beta T cells, which contributed to surface hair loss. Despite these apparently shared traits with AA , lesions were dominated by follicular dystrophy that was atypical of human AA disease, sharing some traits consistent with B6 alopecia and dermatitis. Additionally, juvenile‐onset alopecia was followed by complete, spontaneous recovery of surface hair, without recurrence of hair loss. Prolonging exposure to IL ‐6 prolonged the time to recovery, but once recovered, repeating high‐dose IL ‐6 exposure de novo did not re‐induce alopecia. These data suggest that although substantial molecular and cellular pathways may be shared, functionally similar alopecia disorders can occur via distinct pathological mechanisms.