IL23A and infection: IL-23R signaling subsequently activates STAT3, which maintains RORγt expression and, in turn, promotes the transcription of IL­23R, building up a positive feedback loop, and enhances IL-17 gene transcription (41, 42).In addition to Th17 cells, natural immune cells that express RORγt, such as subsets of γδT cells, NK T (NKT) cells, “natural” Th17 cells, and innate lymphoid cells (ILCs), also respond to IL-23 and have an essential role in both resisting infection and mediating autoimmune pathology (41).