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September 10, 2025Open Access

Loss of TET function in T regulatory cells yields ex-Treg cells biased toward T follicular helper cells, causing autoimmune diseases through autoantibody production

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Authors

KSKazumasa SuzukiLALeo J. Arteaga-VazquezBRBruno Villalobos Reveles

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Overview

Observational analysis reveals ex-Treg cells skew independently toward follicular helper cells, suggesting autoimmune implications.

Key Points

  • Increased methylation in Treg cells leads to their conversion into ex-Treg cells, driving autoimmune disease.
  • Tet2/3-deficient mice exhibited more efficient loss of FOXP3 expression and increased autoantibody production.
  • Histological analysis revealed a significant rise in T follicular helper cells and plasma cells in DKO-severe mice.
  • Impaired TET function in Treg cells suggests a link between DNA methylation and skewed T cell differentiation.

Cite This Study

Suzuki et al. (2025) studied this question.

synapsesocial.com/papers/68c23b08b210217d64782c4ehttps://doi.org/10.1101/2025.08.29.673187
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Assessing the impact of TET2 and TET3 deletion in TCRalpha and TCRbeta repertoire in murine CD4 T cells in physiological and pathophysiological conditions2025
  2. 2Normal Treg homeostasis and suppressive function require both FOXP1 and FOXP42025 · 5 citations
  3. 3TET2 mutations drive cell-autonomous type I interferon production and selective advantage through TRIM4 silencing2025
  4. 4Foxp3 M370I mutation allows the activation of T effector programs in regulatory T cells 37592025
  5. 5Determining FoxP3’s role in hCD8+ iTreg generation, stability, phenotype and function 37312025