JunB is essential for IL-23-dependent pathogenicity of Th17 cells

Zafrul Hasan; Shin-ichi Koizumi; Daiki Sasaki; Hayato Yamada; Nana Arakaki; Yoshitaka Fujihara; Shiho Okitsu; Hiroki Shirahata; Hiroki Ishikawa

doi:10.1038/ncomms15628

Nature Communications (May 2017)

JunB is essential for IL-23-dependent pathogenicity of Th17 cells

Zafrul Hasan,
Shin-ichi Koizumi,
Daiki Sasaki,
Hayato Yamada,
Nana Arakaki,
Yoshitaka Fujihara,
Shiho Okitsu,
Hiroki Shirahata,
Hiroki Ishikawa

Affiliations

Zafrul Hasan: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Shin-ichi Koizumi: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Daiki Sasaki: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Hayato Yamada: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Nana Arakaki: DNA Sequencing Section, Okinawa Institute of Science and Technology Graduate University
Yoshitaka Fujihara: Research Institute for Microbial Diseases, Osaka University
Shiho Okitsu: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Hiroki Shirahata: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University
Hiroki Ishikawa: Immune Signal Unit, Okinawa Institute of Science and Technology Graduate University

DOI: https://doi.org/10.1038/ncomms15628
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 12

Abstract

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T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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