What the study found
The study found a diverse set of fibrosis-associated peptides in the major histocompatibility complex class I immunopeptidome, which is the collection of peptides presented by MHC class I molecules, in human idiopathic pulmonary fibrosis and bleomycin-treated mice. It also found that three candidate peptides reduced fibrosis progression in mice, and that one peptide could trigger human cytotoxic T lymphocytes to kill fibrosis-associated human cells.
Why the authors say this matters
The authors conclude that immunopeptidome profiling provides a robust platform for discovering translatable antifibrotic immunotherapies. The findings indicate that altered peptide presentation in fibrosis may offer therapeutic targets.
What the researchers tested
The researchers characterized MHC class I immunopeptidomes from fibrotic foci in human idiopathic pulmonary fibrosis lung explants and from bleomycin-treated mice. They also used parallel profiling in bleomycin-induced pulmonary fibrosis in mice to computationally prioritize therapeutic targets, then tested candidate peptides through therapeutic vaccination and human cell killing assays.
What worked and what didn't
Therapeutic vaccination with three candidate peptides, MAF116–124, APBB270–78, and TNS3119–127, effectively mitigated fibrosis progression in bleomycin-treated mice. In a separate finding, MAF116–124 elicited specific human cytotoxic T lymphocytes that lysed human idiopathic pulmonary fibrosis-derived myofibroblasts and M2-like macrophages. The abstract does not report unsuccessful candidate peptides or negative results in detail.
What to keep in mind
The findings come from human lung explants, bleomycin-treated mice, and in vitro human cell assays, so the abstract describes evidence from these systems only. The abstract does not provide detailed limitations, safety data, or long-term outcomes.
Key points
- Fibrosis-associated peptides were identified in the MHC class I immunopeptidomes of human and mouse lung fibrosis samples.
- Three candidate peptides reduced fibrosis progression in bleomycin-treated mice after therapeutic vaccination.
- The peptide MAF116–124 triggered human cytotoxic T lymphocytes that killed fibrosis-derived myofibroblasts and M2-like macrophages.
- The authors say immunopeptidome profiling may be a platform for discovering antifibrotic immunotherapies.
Disclosure
- Research title:
- Fibrosis-associated peptides identified as therapeutic targets in lung fibrosis
- Authors:
- Ziyi Bai, Tianxia Lan, Weiqi Hong, Haiying Que, Min Zhu, XJ Xiao, Dandan Wan, Jiayuan Ai, Huang, Jiayu Wang, Qiaonan Hong, Liu Y, Chengxin Xiao, Chengjian Zhao, Xin Wang, Xi Zhang, Ting Yang, Heng Xu, Lunzhi Dai, Charles A. Powell, Luca Richeldi, Fengming Luo, Haohao Dong, 袁勇, Qiang Pu, Xiawei Wei
- Institutions:
- Agostino Gemelli University Polyclinic, Icahn School of Medicine at Mount Sinai, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Sichuan University, Università Cattolica del Sacro Cuore, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University, West China Hospital of Sichuan University
- Publication date:
- 2026-04-20
- OpenAlex record:
- View
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