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<p>Fibrosis is a severe pathological outcome of many chronic diseases, yet the therapeutic potential of targeting the altered major histocompatibility complex (MHC) class I immunopeptidome remains largely unexplored. Here we characterized the MHC class I immunopeptidomes from both fibrotic foci of human idiopathic pulmonary fibrosis lung explants and bleomycin-treated mice, identifying a diverse repertoire of fibrosis-associated peptides. Parallel profiling of bleomycin-induced pulmonary fibrosis in mice enabled the computational prioritization of therapeutic targets. In vivo, therapeutic vaccination with three candidate peptides (MAF<sub>116–124</sub>, APBB2<sub>70–78</sub> and TNS3<sub>119–127</sub>) effectively mitigated fibrosis progression in bleomycin-treated mice. Furthermore, leveraging its evolutionary conservation, we found that MAF<sub>116–124</sub> elicited specific human cytotoxic T lymphocytes that lysed human idiopathic pulmonary fibrosis-derived myofibroblasts and M2-like macrophages. This study indicates that immunopeptidome profiling provides a robust platform for discovering translatable antifibrotic immunotherapies.</p>

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Immunopeptidome profiling in pulmonary fibrosis provides a platform for identifying therapeutic targets

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月20日

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  • Ziyi Bai,
  • Tianxia Lan,
  • Weiqi Hong,
  • Haiying Que,
  • Min Zhu,
  • Xin Xiao,
  • Dandan Wan,
  • Jiayuan Ai,
  • Shaoxiong Huang,
  • Jiayu Wang,
  • Qiaonan Hong,
  • Yanyan Liu,
  • Chengxin Xiao,
  • Chengjian Zhao,
  • Xin Wang,
  • Xiaolong Zhang,
  • Ting Yang,
  • Heng Xu,
  • Lunzhi Dai,
  • Charles A. Powell,
  • Luca Richeldi,
  • Fengming Luo,
  • Haohao Dong,
  • Yong Yuan,
  • Qiang Pu,
  • Xiawei Wei

摘要

Fibrosis is a severe pathological outcome of many chronic diseases, yet the therapeutic potential of targeting the altered major histocompatibility complex (MHC) class I immunopeptidome remains largely unexplored. Here we characterized the MHC class I immunopeptidomes from both fibrotic foci of human idiopathic pulmonary fibrosis lung explants and bleomycin-treated mice, identifying a diverse repertoire of fibrosis-associated peptides. Parallel profiling of bleomycin-induced pulmonary fibrosis in mice enabled the computational prioritization of therapeutic targets. In vivo, therapeutic vaccination with three candidate peptides (MAF116–124, APBB270–78 and TNS3119–127) effectively mitigated fibrosis progression in bleomycin-treated mice. Furthermore, leveraging its evolutionary conservation, we found that MAF116–124 elicited specific human cytotoxic T lymphocytes that lysed human idiopathic pulmonary fibrosis-derived myofibroblasts and M2-like macrophages. This study indicates that immunopeptidome profiling provides a robust platform for discovering translatable antifibrotic immunotherapies.