Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes

Fibroblasts exhibit phenotypic and functional heterogeneity in chronic inflammatory diseases, but how these changes impact immune outcomes remains poorly understood. We identified that a fibroblast population expressing insulin-like growth factor 1 (IGF1) was reduced in patients with inflammatory bowel disease (IBD). Using mouse models of intestinal inflammation, we found cross-talk between IGF1-expressing fibroblasts and group 3 innate lymphoid cells (ILC3s). IGF1 stimulation limited the ability of ILC3s to produce C-X-C motif chemokine ligand 10 (CXCL10) and recruit plasmacytoid dendritic cells (pDCs) to restrain gut inflammation. We propose that this regulatory pathway is conserved in human ILC3s but may become impaired in IBD. Our results define that anti-inflammatory fibroblasts safeguard the gut through regulation of an innate lymphocyte–pDC axis.

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Journal
Science
Published
2026-09-24
DOI
https://doi.org/10.1126/science.aei0062
Primary Topic
IL-33, ST2, and ILC Pathways
Type
article
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Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes

Hua Tang, Gregory F. Sonnenberg, Ruixiao Liu, Minhao Yu et al.
Science
IL-33, ST2, and ILC Pathways
article

Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes

Hua Tang, Gregory F. Sonnenberg, Ruixiao Liu, Minhao Yu, Shanhao Jin, Coco Chu, Zhijun Cao, Lan Kang, Xiaoyu Hu, Lei Zhou, Qiang Wang, Chong Liu, Xitao Xu, Quan Zhang, Yu Lu, Wenxuan Xu, Yu Zhou, Z. Tang, Zhijie Gu, Hongzhi Liu, Boyuan Chen, Qingxia Lin, Zhe Cui, Yanting Zhang, Yi Wang
article en

Abstract

Fibroblasts exhibit phenotypic and functional heterogeneity in chronic inflammatory diseases, but how these changes impact immune outcomes remains poorly understood. We identified that a fibroblast population expressing insulin-like growth factor 1 (IGF1) was reduced in patients with inflammatory bowel disease (IBD). Using mouse models of intestinal inflammation, we found cross-talk between IGF1-expressing fibroblasts and group 3 innate lymphoid cells (ILC3s). IGF1 stimulation limited the ability of ILC3s to produce C-X-C motif chemokine ligand 10 (CXCL10) and recruit plasmacytoid dendritic cells (pDCs) to restrain gut inflammation. We propose that this regulatory pathway is conserved in human ILC3s but may become impaired in IBD. Our results define that anti-inflammatory fibroblasts safeguard the gut through regulation of an innate lymphocyte–pDC axis.

ScienceVol. 393(6818)
Zhejiang Chinese Medical University (CN), University of California, Los Angeles (US), Shanxi Medical University (CN), Shanghai Jiao Tong University (CN), Capital Medical University (CN), Cornell University (US), Renji Hospital (CN), Westlake University (CN), Beijing Friendship Hospital (CN), Second Affiliated Hospital of Zhejiang University (CN), Center for Life Sciences (CN), Shandong First Medical University (CN), Zhejiang University (CN), Yangzhou University (CN), Tsinghua University (CN)
Good health and well-being
Openalex Percentile: Top 18%
IL-33, ST2, and ILC Pathways
DOISourceOpenAlex
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