IKZF1 and IKAROS Overexpression Contributes to the Pathogenesis of Alopecia Areata

    Y. Arakawa, R. Tamagawa-Mineoka, M. Nakanishi, H. Nishigaki, M.Y. Ueta, N. Katoh
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    TLDR Too much IKZF1 and Ikaros protein may cause alopecia areata.
    The study investigates the role of IKZF1 and its encoded protein IKAROS in the pathogenesis of alopecia areata (AA). Using a transgenic mouse model (Ikzf1 Tg) that overexpresses IKZF1, researchers observed AA-like alopecia lesions, increased expression of the NKG2D ligand H60, and infiltration of CD8+NKG2D+ T cells. Additionally, there was significant upregulation of inflammatory mediators such as IL-15, TNF-a, and various CXCL chemokines in the alopecia lesions of these mice. Hair regrowth was achieved through corticosteroid injections. Immuno-histological analysis of human scalp tissues revealed overexpression of IKAROS in AA patients compared to non-AA controls. The findings suggest that IKZF1 and IKAROS contribute to the development of AA.
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