Establishing a model for mouse alopecia areata and identifying its characteristics

Abstract

Alopecia areata (AA) is an autoimmune skin disease, causing hair loss on the scalp. This is a relatively common disease, accounting for 1.7 percent of the world's population. However, studies on AA have been limited due to difficulty of establishing animal model. Here, we have established an experimental murine model of AA using C3H/HeJ mice in our laboratory via cultured cell transfer method. We revealed that the transferred cells obtained from skin-draining lymph node cells (LNCs) of an AA-developed mice can successfully induce AA as about 74%, and found that the major population are NKG2D+CD8+ T cells. C3H/HeJ lesion analysis identified that NKG2D+ Tbet+ Eomes- CD8+ T cells were significantly infiltrated the epithelial layer of hair follicles with an increase in total cellularity. Next, we tried to treat AA by topical administration of Janus kinase (JAK) inhibitor, which inhibit effector molecules and signaling of downstream of IFN-γ and γc cytokine receptors, but confirmed that it would recur again when treatment was stopped. We tried to study that Tregs could cure the AA permanently by intradermal injecting hIL2/5344.111 complex (5344c) via IL-2Rα (CD25) signaling transmission. However, unfortunately, it was confirmed that these approaches also could not permanently cure AA. Although our study has not yet fully elucidated the exact mechanism for treating the AA disease, we were able to characterize the major cell population that cause this onset, and I have set up a new murine disease model in vivo. In this respect, we expect that it will be able to spur research using our model in the future.