Induction of alopecia areata in C3H/HeJ mice using polyinosinic-polycytidylic acid (poly[I:C]) and interferon-gamma

• Published in: Scientific reports 2018-08, Vol.8 (1), p.12518-8, Article 12518
• Main Authors: Shin, Jung-Min, Choi, Dae-Kyoung, Sohn, Kyung-Cheol, Koh, Jung-Woo, Lee, Young Ho, Seo, Young-Joon, Kim, Chang Deok, Lee, Jeung-Hoon, Lee, Young
• Format: Article
• Language: English
• Subjects: 13/1; 13/21; 13/51; 631/80/304; 64; 64/60; 692/699/4033; 82/80; Alopecia; Animal diseases; Animal models; Baldness; CD4 antigen; CD8 antigen; CXCL10 protein; CXCL11 protein; Double-stranded RNA; Follicles; Hair; Hair loss; Humanities and Social Sciences; IL-1β; Infiltration; Inflammasomes; Innate immunity; Lesions; Lymphocytes T; multidisciplinary; Pathogenesis; Pathophysiology; Polyinosinic:polycytidylic acid; Science; Science (multidisciplinary); Skin; Therapeutic applications; γ-Interferon
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-30997-3

Alopecia areata (AA) is a chronic, relapsing hair-loss disorder that is considered to be a T-cell-mediated autoimmune disease. Several animal models for AA have been created to investigate the pathophysiology and screen for effective therapeutic targets. As C3H/HeJ mice develop AA spontaneously in a low frequency, a novel animal model is needed to establish an AA-like condition faster and more conveniently. In this study, we present a novel non-invasive AA rodent model that avoids skin or lymph-node cell transfer. We simply injected C3H/HeJ mice subcutaneously with interferon-gamma (IFNγ) along with polyinosinic:polycytidylic acid (poly[I:C]), a synthetic dsRNA, to initiate innate immunity via inflammasome activation. Approximately 80% of the IFNγ and poly(I:C) co-injected mice showed patchy AA lesions after 8 weeks. None of the mice displayed hair loss in the IFNγ or poly(I:C) solely injection group. Immunohistochemical staining of the AA lesions revealed increased infiltration of CD4 + and CD8 + cells infiltration around the hair follicles. IFNγ and poly(I:C) increased the expression of NLRP3, IL-1β, CXCL9, CXCL10, and CXCL11 in mouse skin. Taken together, these findings indicate a shorter and more convenient means of AA animal model induction and demonstrate that inflammasome-activated innate immunity is important in AA pathogenesis.