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<p>Immune-stromal crosstalk governs tissue fibrosis, which is marked by dysregulated extracellular matrix (ECM) production and aberrant vasculature. Here, we investigate how γδ T cell interactions with stromal cells shape fibrosis in the foreign body response in a murine biomaterial implant model. During the acute reaction, type-1 (γδIFNγ) and type-17 (γδ17) γδ T cell subsets accumulate at the implant site. While γδIFNγ cells decrease as fibrosis progresses, activated γδ17 cells persist as dominant interleukin-17 producers. The γδ17 cell compartment expands with aging and high-fat diet, both factors associated with chronic inflammation and fibrosis. Fibroblasts co-cultured with γδ17 cells exhibit increased expression of collagen genes and intercellular communication inference links γδ T cell ligands to activation of ECM remodeling and vascular development programs in fibroblasts and endothelial cells. Finally, genetic deletion of γδ T cells in mice alters expression of ECM components and increases vessel size within the fibrotic matrix. Altogether, our findings implicate γδ T cells in regulating stromal cell behavior to modulate composition and vascularity of fibrotic tissues.</p>

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γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月17日

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  • Anna Ruta,
  • Kavita Krishnan,
  • JiWon Woo,
  • Joscelyn C. Mejías,
  • Elise F. Gray-Gaillard,
  • David R. Maestas Jr.,
  • Helen Hieu Nguyen,
  • Alexandra N. Rindone,
  • Christopher Cherry,
  • Michael Patatanian,
  • Frank Haoning Yu,
  • Brenda Yang,
  • Connor Amelung,
  • Christina D. King,
  • Birgit Schilling,
  • Sharon Gerecht,
  • Elana J. Fertig,
  • Locke Davenport Huyer,
  • Drew M. Pardoll,
  • Jennifer H. Elisseeff

摘要

Immune-stromal crosstalk governs tissue fibrosis, which is marked by dysregulated extracellular matrix (ECM) production and aberrant vasculature. Here, we investigate how γδ T cell interactions with stromal cells shape fibrosis in the foreign body response in a murine biomaterial implant model. During the acute reaction, type-1 (γδIFNγ) and type-17 (γδ17) γδ T cell subsets accumulate at the implant site. While γδIFNγ cells decrease as fibrosis progresses, activated γδ17 cells persist as dominant interleukin-17 producers. The γδ17 cell compartment expands with aging and high-fat diet, both factors associated with chronic inflammation and fibrosis. Fibroblasts co-cultured with γδ17 cells exhibit increased expression of collagen genes and intercellular communication inference links γδ T cell ligands to activation of ECM remodeling and vascular development programs in fibroblasts and endothelial cells. Finally, genetic deletion of γδ T cells in mice alters expression of ECM components and increases vessel size within the fibrotic matrix. Altogether, our findings implicate γδ T cells in regulating stromal cell behavior to modulate composition and vascularity of fibrotic tissues.