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<p>The co-inhibitory receptor TIGIT suppresses excessive immune responses in autoimmune conditions while also restraining antitumor immunity. In viral infections, TIGIT alone does not affect viral control but has been shown to limit tissue pathology. However, the underlying mechanisms are incompletely understood. Here we found TIGIT<sup>+</sup> T cells to express not only an immunoregulatory gene signature but also a tissue repair gene signature. Specifically, after viral infection, TIGIT directly drives expression of the tissue growth factor amphiregulin (Areg), which is strongly reduced in the absence of TIGIT. We identified regulatory T (T<sub>reg</sub>) cells, but not CD8<sup>+</sup> T cells, as the critical T cell subset mediating these tissue-protective effects. In T<sub>reg</sub> cells, TIGIT engagement after T cell antigen receptor stimulation induces the transcription factor Blimp-1, which then promotes Areg production and tissue repair. Thus, we uncovered a nonclassical function of the co-inhibitory receptor TIGIT, wherein it not only limits immune pathology by suppressing the immune response but also actively fosters tissue regeneration by inducing the tissue growth factor Areg in T cells.</p>

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The co-inhibitory receptor TIGIT promotes tissue-protective functions in T cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月15日

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  • Camilla Panetti,
  • Rahel Daetwyler,
  • Anja Moncsek,
  • Nikolaos Patikas,
  • Andreas Agrafiotis,
  • Adelynn Tang,
  • Francesco Andreata,
  • Valeria Fumagalli,
  • Jean De Lima,
  • Lifen Wen,
  • Carolyn G. King,
  • Ajithkumar Vasanthakumar,
  • Matteo Iannacone,
  • Axel Kallies,
  • Alexander Yermanos,
  • Martin Hemberg,
  • Nicole Joller

摘要

The co-inhibitory receptor TIGIT suppresses excessive immune responses in autoimmune conditions while also restraining antitumor immunity. In viral infections, TIGIT alone does not affect viral control but has been shown to limit tissue pathology. However, the underlying mechanisms are incompletely understood. Here we found TIGIT+ T cells to express not only an immunoregulatory gene signature but also a tissue repair gene signature. Specifically, after viral infection, TIGIT directly drives expression of the tissue growth factor amphiregulin (Areg), which is strongly reduced in the absence of TIGIT. We identified regulatory T (Treg) cells, but not CD8+ T cells, as the critical T cell subset mediating these tissue-protective effects. In Treg cells, TIGIT engagement after T cell antigen receptor stimulation induces the transcription factor Blimp-1, which then promotes Areg production and tissue repair. Thus, we uncovered a nonclassical function of the co-inhibitory receptor TIGIT, wherein it not only limits immune pathology by suppressing the immune response but also actively fosters tissue regeneration by inducing the tissue growth factor Areg in T cells.