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<p>Peripherally induced regulatory T (pT<sub>reg</sub>) cells play an essential role in establishing immune tolerance to gut microbiota and food antigens. A subset of RORγt-expressing antigen-presenting cells, Thetis cell subset IV (TC IV), plays an essential role in intestinal tolerance. However, the transcription factors governing the differentiation of this subset remain unclear. Here we show that Runx–CBFβ complexes regulate the development of specific TC subsets. Mice lacking CBFβ2 exhibited loss of TC II, III and IV, with loss of RORγt<sup>+</sup> pT<sub>reg</sub> cells. Transgenic CBFβ2 expression by <i>Cd11c</i>-Cre restored TC IV and RORγt<sup>+</sup> pT<sub>reg</sub> cell differentiation in CBFβ2-deficient mice. Conditional inactivation of <i>Runx1</i> and <i>Runx3</i> by <i>Cd11c</i>-Cre selectively impaired TC III and IV. Conversely <i>Cd11c-</i>Cre-driven transgenic Runx expression enhanced TC IV differentiation and thus RORγt<sup>+</sup> pT<sub>reg</sub> cell induction. These findings establish a critical pathway for TC IV differentiation and provide new insights into therapeutic interventions to promote RORγt<sup>+</sup> pT<sub>reg</sub> cell induction in autoimmune diseases.</p>

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Runx–CBFβ regulates the development of tolerogenic Thetis cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月19日

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  • Chihiro Ogawa,
  • Chengcheng Zou,
  • Yoselin A. Paucar Iza,
  • Motoi Yamashita,
  • Tyler Park,
  • Junji Harada,
  • Naoko Satoh-Takayama,
  • Masahiko Kuroda,
  • Chrysothemis C. Brown,
  • Ichiro Taniuchi

摘要

Peripherally induced regulatory T (pTreg) cells play an essential role in establishing immune tolerance to gut microbiota and food antigens. A subset of RORγt-expressing antigen-presenting cells, Thetis cell subset IV (TC IV), plays an essential role in intestinal tolerance. However, the transcription factors governing the differentiation of this subset remain unclear. Here we show that Runx–CBFβ complexes regulate the development of specific TC subsets. Mice lacking CBFβ2 exhibited loss of TC II, III and IV, with loss of RORγt+ pTreg cells. Transgenic CBFβ2 expression by Cd11c-Cre restored TC IV and RORγt+ pTreg cell differentiation in CBFβ2-deficient mice. Conditional inactivation of Runx1 and Runx3 by Cd11c-Cre selectively impaired TC III and IV. Conversely Cd11c-Cre-driven transgenic Runx expression enhanced TC IV differentiation and thus RORγt+ pTreg cell induction. These findings establish a critical pathway for TC IV differentiation and provide new insights into therapeutic interventions to promote RORγt+ pTreg cell induction in autoimmune diseases.