JunB plays a crucial role in development of regulatory T cells by promoting IL-2 signaling

• DOI: 10.1038/s41385-019-0182-0
• Publication Date: 2019-07-08T06:02:54Z
• Authors: Takaharu Katagiri; Soh Yamazaki; Yuto Fukui; Kotaro Aoki; Hideo Yagita; Takashi Nishina; Tetuo Mikami; Sayaka Katagiri; Ayako Shiraishi; Soichiro Kimura; Kazuhiro Tateda; Hideki Sumimoto; Shogo Endo; Hideto Kameda; Hiroyasu Nakano
• Keywords: JUNB; Adoptive Cell Transfer

The AP-1 transcription factor JunB plays crucial roles in multiple biological processes, including placental formation and bone homeostasis. We recently reported that is essential for development of Th17 cells, thus Junb-deficient mice are resistant to experimental autoimmune encephalomyelitis. However, the role CD4+ T cells under other inflammatory disease conditions unknown. Here we show lacking (Junbfl/flCd4-Cre mice) were more susceptible dextran sulfate sodium (DSS)-induced colitis because impaired regulatory (Treg) cells. Production interleukin (IL)-2 expression CD25, a high affinity IL-2 receptor component, decreased vitro vivo. Naive from Junbfl/flCd4-Cre failed differentiate into Treg absence exogenously added vitro. A mixed marrow transfer experiment revealed defective was not rescued by co-transferred wild-type indicating significance cell-intrinsic defect. Injection IL-2-anti-IL-2 antibody complexes induced expansion alleviated DSS-induced mice. Thus facilitating signaling.