Bach2–Batf interactions control Th2-type immune response by regulating the IL-4 amplification loop

Makoto Kuwahara, Wataru Ise, Mizuki Ochi, Junpei Suzuki, Kohei Kometani, Saho Maruyama, Maya Izumoto, Akira Matsumoto, Nobuaki Takemori, Ayako Takemori, Kenta Shinoda, Toshinori Nakayama, Osamu Ohara, Masaki Yasukawa, Tatsuya Sawasaki, Tomohiro Kurosaki and Masakatsu Yamashita ()
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Makoto Kuwahara: Graduate School of Medicine, Ehime University, Shitsukawa
Wataru Ise: WPI Immunology Frontier Research Center
Mizuki Ochi: Graduate School of Medicine, Ehime University, Shitsukawa
Junpei Suzuki: Translational Research Center, Ehime University Hospital, Shitsukawa
Kohei Kometani: Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences
Saho Maruyama: Graduate School of Medicine, Ehime University, Shitsukawa
Maya Izumoto: Graduate School of Medicine, Ehime University, Shitsukawa
Akira Matsumoto: Graduate School of Medicine, Ehime University, Shitsukawa
Nobuaki Takemori: Proteo-Science Center, Ehime University
Ayako Takemori: Proteo-Science Center, Ehime University
Kenta Shinoda: Graduate School of Medicine
Toshinori Nakayama: Graduate School of Medicine
Osamu Ohara: Human DNA Analysis Group, Kazusa DNA Research Institute
Masaki Yasukawa: Clinical Immunology and Infectious Diseases, Graduate School of Medicine, Ehime University, Shitsukawa
Tatsuya Sawasaki: Proteo-Science Center, Ehime University
Tomohiro Kurosaki: WPI Immunology Frontier Research Center
Masakatsu Yamashita: Graduate School of Medicine, Ehime University, Shitsukawa

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Although Bach2 has an important role in regulating the Th2-type immune response, the underlying molecular mechanisms remain unclear. We herein demonstrate that Bach2 associates with Batf and binds to the regulatory regions of the Th2 cytokine gene loci. The Bach2–Batf complex antagonizes the recruitment of the Batf–Irf4 complex to AP-1 motifs and suppresses Th2 cytokine production. Furthermore, we find that Bach2 regulates the Batf and Batf3 expressions via two distinct pathways. First, Bach2 suppresses the maintenance of the Batf and Batf3 expression through the inhibition of IL-4 production. Second, the Bach2–Batf complex directly binds to the Batf and Batf3 gene loci and reduces transcription by interfering with the Batf–Irf4 complex. These findings suggest that IL-4 and Batf form a positive feedback amplification loop to induce Th2 cell differentiation and the subsequent Th2-type immune response, and Bach2–Batf interactions are required to prevent an excessive Th2 response.

Date: 2016
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DOI: 10.1038/ncomms12596

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