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Piezo1 channels restrain regulatory T cells but are dispensable for effector CD4+ T cell responses.

  • Author(s): Jairaman, Amit
  • Othy, Shivashankar
  • Dynes, Joseph L
  • Yeromin, Andriy V
  • Zavala, Angel
  • Greenberg, Milton L
  • Nourse, Jamison L
  • Holt, Jesse R
  • Cahalan, Stuart M
  • Marangoni, Francesco
  • Parker, Ian
  • Pathak, Medha M
  • Cahalan, Michael D
  • et al.
Abstract

T lymphocytes encounter complex mechanical cues during an immune response. The mechanosensitive ion channel, Piezo1, drives inflammatory responses to bacterial infections, wound healing, and cancer; however, its role in helper T cell function remains unclear. In an animal model for multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we found that mice with genetic deletion of Piezo1 in T cells showed diminished disease severity. Unexpectedly, Piezo1 was not essential for lymph node homing, interstitial motility, Ca2+ signaling, T cell proliferation, or differentiation into proinflammatory T helper 1 (TH1) and TH17 subsets. However, Piezo1 deletion in T cells resulted in enhanced transforming growth factor-β (TGFβ) signaling and an expanded pool of regulatory T (Treg) cells. Moreover, mice with deletion of Piezo1 specifically in Treg cells showed significant attenuation of EAE. Our results indicate that Piezo1 selectively restrains Treg cells, without influencing activation events or effector T cell functions.

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