[HTML][HTML] Th9 cell development requires a BATF-regulated transcriptional network

R Jabeen, R Goswami, O Awe… - The Journal of …, 2013 - Am Soc Clin Investig
R Jabeen, R Goswami, O Awe, A Kulkarni, ET Nguyen, A Attenasio, D Walsh, MR Olson
The Journal of clinical investigation, 2013Am Soc Clin Investig
T helper 9 (Th9) cells are specialized for the production of IL-9, promote allergic
inflammation in mice, and are associated with allergic disease in humans. It has not been
determined whether Th9 cells express a characteristic transcriptional signature. In this study,
we performed microarray analysis to identify genes enriched in Th9 cells compared with
other Th subsets. This analysis defined a transcriptional regulatory network required for the
expression of a subset of Th9-enriched genes. The activator protein 1 (AP1) family …
T helper 9 (Th9) cells are specialized for the production of IL-9, promote allergic inflammation in mice, and are associated with allergic disease in humans. It has not been determined whether Th9 cells express a characteristic transcriptional signature. In this study, we performed microarray analysis to identify genes enriched in Th9 cells compared with other Th subsets. This analysis defined a transcriptional regulatory network required for the expression of a subset of Th9-enriched genes. The activator protein 1 (AP1) family transcription factor BATF (B cell, activating transcription factor–like) was among the genes enriched in Th9 cells and was required for the expression of IL-9 and other Th9-associated genes in both human and mouse T cells. The expression of BATF was increased in Th9 cultures derived from atopic infants compared with Th9 cultures from control infants. T cells deficient in BATF expression had a diminished capacity to promote allergic inflammation compared with wild-type controls. Moreover, mouse Th9 cells ectopically expressing BATF were more efficient at promoting allergic inflammation than control transduced cells. These data indicate that BATF is a central regulator of the Th9 phenotype and contributes to the development of allergic inflammation.
The Journal of Clinical Investigation