TGFB1 and autoimmune encephalitis: Studies have shown that IL-23 induces TGFβ3 rather than TGFβ1, which combined with IL-6 leads to development of pathogenic Th17 cells, which are both functionally and transcriptionally distinct from homeostatic, non-pathogenic Th17 cells induced by TGFβ1, as shown in experimental autoimmune encephalitis models (44, 45).