@article{oai:oist.repo.nii.ac.jp:00000925,
 author = {Koizumi, Shin-ichi and Sasaki, Daiki and Hsieh, Tsung-Han and Taira, Naoyuki and Arakaki, Nana and Yamasaki, Shinichi and Wang, Ke and Sarkar, Shukla and Shirahata, Hiroki and Miyagi, Mio and Ishikawa, Hiroki},
 issue = {1},
 journal = {Nature Communications},
 month = {Dec},
 note = {Foxp3-expressing CD4(+) regulatory T (Treg) cells need to differentiate into effector Treg (eTreg) cells to maintain immune homeostasis. T-cell receptor (TCR)-dependent induction of the transcription factor IRF4 is essential for eTreg differentiation, but how IRF4 activity is regulated in Treg cells is still unclear. Here we show that the AP-1 transcription factor, JunB, is expressed in eTreg cells and promotes an IRF4-dependent transcription program. Mice lacking JunB in Treg cells develop multi-organ autoimmunity, concomitant with aberrant activation of T helper cells. JunB promotes expression of Treg effector molecules, such as ICOS and CTLA4, in BATF-dependent and BATF-independent manners, and is also required for homeostasis and suppressive functions of eTreg. Mechanistically, JunB facilitates the accumulation of IRF4 at a subset of IRF4 target sites, including those located near Icos and Ctla4. Thus, JunB is a critical regulator of IRF4-dependent Treg effector programs, highlighting important functions for AP-1 in Treg-mediated immune homeostasis.},
 title = {JunB regulates homeostasis and suppressive functions of effector regulatory T cells},
 volume = {9},
 year = {2018}
}