Fig. 1
From: What’s old is new again: Batf transcription factors and Th9 cells
TL1A enhances the development and inflammatory function of Th9 cells via BATF3. CD4+ T helper (TH) cells encountering antigen at mucosal surfaces, such as the intestinal tract and lung, are exposed to the TNF family co-stimulatory cytokine TL1A derived from myeloid and epithelial cells. TL1A binds to its cognate receptor, DR3, on TH cells, which, in the presence of Th9-polarizing cytokines (TGFβ1 and IL-4) promotes enhanced expression of the AP-1 family transcription factors, BATF and BATF3, in a STAT6-dependent manner. Once expressed, BATF and BATF3 bind to regulatory elements in the Il9 promoter, leading to increased histone acetylation, IRF4 binding and Il9 gene expression. Accordingly, TL1A enhances, whereas loss of BATF3 represses, Th9-driven mucosal inflammation in vivo
