GPR171 restrains intestinal inflammation by suppressing FABP5-mediated Th17 cell differentiation and lipid metabolism
GPR171 deficiency promotes Th17 cell differentiation and causes lipid metabolism perturbation, contributing to intestinal inflammation in a FABP5-dependent manner. Target therapy (eg, BigLEN-Fc) represents a novel therapeutic approach for IBD treatment.
Authors
- Jian Lin (ORCID: https://orcid.org/0000-0003-1265-5314)
- Fushun Kou (ORCID: https://orcid.org/0000-0003-1841-3324)
- Yao Ding (ORCID: https://orcid.org/0000-0003-3493-8526)
- Dengfeng Kang
- Zhanju Liu (ORCID: https://orcid.org/0000-0002-0326-543X)
- Xiaohan Wu (ORCID: https://orcid.org/0000-0002-0050-7616)
- Ting Ban
- Qing Zhang (ORCID: https://orcid.org/0000-0003-0404-5743)
- Xiaoyu Li (ORCID: https://orcid.org/0000-0001-6696-7837)
- Ai Li (ORCID: https://orcid.org/0000-0003-1510-4729)
- Junxiang Li (ORCID: https://orcid.org/0000-0001-8452-8029)
- Han Gao (ORCID: https://orcid.org/0000-0002-6157-0811)
- Zhongsheng Feng
- Jinghan Hua (ORCID: https://orcid.org/0009-0003-5618-1234)
Institutions
- Tongji University (CN)
- Beijing University of Chinese Medicine (CN)
- Shanghai Tenth People's Hospital (CN)
- Regend Therapeutics (China) (CN)
Publication Details
- Journal
- Gut
- Published
- 2025-03-12
- DOI
- https://doi.org/10.1136/gutjnl-2024-334010
- Citations
- 12
- Primary Topic
- Immune Cell Function and Interaction
- Type
- article
- Field-Weighted Citation Impact
- 9.57
Funders
- National Natural Science Foundation of China