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ORIGINAL RESEARCH article

Front. Immunol.
Sec. T Cell Biology
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1440918

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis

Provisionally accepted
Masaaki Okamoto Masaaki Okamoto 1Ayumi Kuratani Ayumi Kuratani 1Daisuke Okuzaki Daisuke Okuzaki 1Naganori Kamiyama Naganori Kamiyama 2Takashi Kobayashi Takashi Kobayashi 2Miwa Sasai Miwa Sasai 1Masahiro Yamamoto Masahiro Yamamoto 3*
  • 1 Research Institute for Microbial Diseases, Osaka University, Suita, Ōsaka, Japan
  • 2 Faculty of Medicine, Oita University, Yufu, Oita, Japan
  • 3 Osaka University, Suita, Japan

The final, formatted version of the article will be published soon.

    Bleomycin (BLM) induces lung injury, leading to inflammation and pulmonary fibrosis. Regulatory T cells (Tregs) maintain self-tolerance and control host immune responses. However, little is known about their involvement in the pathology of pulmonary fibrosis. Here we show that a unique Treg subset expressing trefoil factor family 1 (Tff1) emerges in the BLM-injured lung. These Tff1expressing Tregs (Tff1-Tregs) were induced by IL-33. Moreover, although Tff1 ablation in Tregs did not change the pathological condition, selective ablation of Tff1-Tregs using an intersectional genetic method promoted pro-inflammatory features of macrophages in the injured lung and exacerbated the fibrosis. Taken together, our study revealed the presence of a unique Treg subset expressing Tff1 in BLM-injured lungs and their critical role in the injured lung to ameliorate fibrosis.

    Keywords: Bleomycin, Fibrosis, Treg, TFF1, VeDTR

    Received: 30 May 2024; Accepted: 12 Aug 2024.

    Copyright: © 2024 Okamoto, Kuratani, Okuzaki, Kamiyama, Kobayashi, Sasai and Yamamoto. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Masahiro Yamamoto, Osaka University, Suita, Japan

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