Th1 effector CD4 T cells rely on IFN-g production to induce Alopecia areata
Alopecia areata (AA) is an autoimmune disease that is characterized by hair loss clinically and peribulbar infiltration of CD8 and CD4 T cells histologically. Prior studies have focused on the role of CD8 T cells in the development of AA; however, the role of CD4 T cells is unclear. Here, we demonstrate that CD4 T cells from the skin draining lymph nodes (SDLN) of AA mice could transfer disease into recipient mice. Further, these cells exhibited a T-helper type 1 (Th1) effector transcriptional and phenotypic profile. Pathogenic activity of these CD4 T cells was dependent upon the presence of endogenous CD8 T cells and host IFN-g signaling. Targeted removal of CD4 T cell-mediated production of IFN-g abrogated the ability of this cell population to transfer disease. Together, our study provides mechanistic insights into pathways that lead to AA development, heightening our understanding of the disease and inviting studies into exploring novel therapeutic strategies for human patients. Overall design: RNA-seq profiling of live TCRß+CD4+ T cells that were sorted (Becton Dickinson FACS Aria Fusion) from skin draining lymph nodes (SDLNs) of unaffected (UA) and alopeica areata (AA) affected C3H/HeJ mice.