056 IKZF1 and IKAROS overexpression contributes to the pathogenesis of alopecia areata

Background: IKAROS, encoded by Ikaros Family Zinc Finger 1 (IKZF1), is a zinc finger transcription factor and critical regulator of hematopoiesis. We previously found that human epidermis expressed IKZF1. In addition, we generated K5-Ikzf1-EGFP transgenic mice (Ikzf1 Tg) introducing the IKZF1 isoform into cells expressing keratin 5 which developed dermatitis also patchy alopecia. A previous in vitro study suggested possible pathological functions alopecia areata (AA). However, there has been no detailed investigation its function vivo studies or expression hair follicle tissue AA. Methods: examined visual histological findings skin lesions Ikzf1 Tg wild-type (WT) mRNA inflammation mediators. Moreover, IKAROS scalp tissues. Results: AA like visually histologically mice. Immuno-histologically, NKG2D ligand H60 was strongly infiltration CD8+NKG2D+ T were observed Tg. IL-15, TNF-a, CXCL1, CXCL9, CXCL10, CXCL11.STAT1, STAT3, JAK1, JAK3 significantly upregulated compared to wild type (WT). Hair regrowth occurred corticosteroid injection. Immuno-histological analysis revealed Ikaros; protein gene over follicles patients non-AA controls. Conclusion: Our shows relevance support hypothesis participates pathogenesis