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JunB regulates homeostasis and suppressive functions of effector regulatory T cells

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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)

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.

Suggested Citation

  • Shin-ichi Koizumi & Daiki Sasaki & Tsung-Han Hsieh & Naoyuki Taira & Nana Arakaki & Shinichi Yamasaki & Ke Wang & Shukla Sarkar & Hiroki Shirahata & Mio Miyagi & Hiroki Ishikawa, 2018. "JunB regulates homeostasis and suppressive functions of effector regulatory T cells," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07735-4
    DOI: 10.1038/s41467-018-07735-4
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    Cited by:

    1. Kami Pekayvaz & Alexander Leunig & Rainer Kaiser & Markus Joppich & Sophia Brambs & Aleksandar Janjic & Oliver Popp & Daniel Nixdorf & Valeria Fumagalli & Nora Schmidt & Vivien Polewka & Afra Anjum & , 2022. "Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection," Nature Communications, Nature, vol. 13(1), pages 1-21, December.
    2. Sang T. Kim & Yanshuo Chu & Mercy Misoi & Maria E. Suarez-Almazor & Jean H. Tayar & Huifang Lu & Maryam Buni & Jordan Kramer & Emma Rodriguez & Zulekha Hussain & Sattva S. Neelapu & Jennifer Wang & Am, 2022. "Distinct molecular and immune hallmarks of inflammatory arthritis induced by immune checkpoint inhibitors for cancer therapy," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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