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

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 Tff1-expressing 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.

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Publication Details

Journal
Frontiers in Immunology
Published
2024-09-02
DOI
https://doi.org/10.3389/fimmu.2024.1440918
Citations
8
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
3.35
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article

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

Daisuke Okuzaki, Ayumi Kuratani, Miwa Sasai, Naganori Kamiyama et al.
8 citations
Frontiers in Immunology
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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article

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

Daisuke Okuzaki, Ayumi Kuratani, Miwa Sasai, Naganori Kamiyama, Masahiro Yamamoto, Takashi Kobayashi, Masaaki Okamoto
article en
8 citations

Abstract

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 Tff1-expressing 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.

Frontiers in ImmunologyVol. 15
Oita University (JP), Osaka International University (JP), The University of Osaka (JP)
Good health and well-being
Openalex Percentile: Top 7%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
3.35
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