JunB regulates homeostasis and suppressive functions of effector regulatory T cells

Shin-ichi Koizumi, Daiki Sasaki, Tsung-Han Hsieh, Naoyuki Taira, Nana Arakaki, Shinichi Yamasaki, Ke Wang, Shukla Sarkar, Hiroki Shirahata, Mio Miyagi and Hiroki Ishikawa ()
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Shin-ichi Koizumi: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Daiki Sasaki: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Tsung-Han Hsieh: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Naoyuki Taira: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Nana Arakaki: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Shinichi Yamasaki: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Ke Wang: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Shukla Sarkar: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Hiroki Shirahata: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Mio Miyagi: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha
Hiroki Ishikawa: Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-07735-4

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