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肺组织中表达 Tff1 的调节性 T 细胞可预防博来霉素诱导的肺纤维化恶化。

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

机构信息

Department of Immunoparasitology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.

Laboratory of Immunoparasitology, World Premier International Research Center Initiative Immunology Frontier Research Center, Osaka University, Suita, Japan.

出版信息

Front Immunol. 2024 Sep 2;15:1440918. doi: 10.3389/fimmu.2024.1440918. eCollection 2024.

DOI:10.3389/fimmu.2024.1440918
PMID:39286257
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11402662/
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.

摘要

博来霉素（BLM）可引起肺损伤，导致炎症和肺纤维化。调节性 T 细胞（Tregs）可维持自身耐受并控制宿主免疫反应。然而，其在肺纤维化发病机制中的作用知之甚少。本研究显示，BLM 损伤肺中出现了一种表达三叶因子家族 1（Tff1）的独特 Treg 亚群。这些表达 Tff1 的 Tregs（Tff1-Tregs）由 IL-33 诱导产生。此外，尽管 Treg 中 Tff1 的缺失并未改变病理状况，但使用交叉遗传方法选择性消融 Tff1-Tregs 可促进损伤肺中巨噬细胞的促炎特征，并加重纤维化。综上所述，本研究揭示了 BLM 损伤肺中存在表达 Tff1 的独特 Treg 亚群，以及它们在改善纤维化方面对损伤肺的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/88646e54266d/fimmu-15-1440918-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/cbfcaf2405dd/fimmu-15-1440918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/144eb3f4f8c9/fimmu-15-1440918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/51f5f9bed03a/fimmu-15-1440918-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/37d6a014b259/fimmu-15-1440918-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/aa03c3783674/fimmu-15-1440918-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/88646e54266d/fimmu-15-1440918-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/cbfcaf2405dd/fimmu-15-1440918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/144eb3f4f8c9/fimmu-15-1440918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/51f5f9bed03a/fimmu-15-1440918-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/37d6a014b259/fimmu-15-1440918-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/aa03c3783674/fimmu-15-1440918-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31ad/11402662/88646e54266d/fimmu-15-1440918-g006.jpg

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