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For antigen-specific effector or Foxp3^(+) regulatory T cell fate, cyclin-dependent kinases hold the trump card

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摘要 Forkhead box p3^(+)(Foxp3^(+))regulatory T cells(Tregs)are indispensable for immune homeostasis and for maintaining immune tolerance.Several studies have confirmed that injection of a T cell population depleted of Tregs causes autoimmunity,rejection of grafts and inflammatory disorders,whereas reconstitution with Tregs inhibits these pathogenic processes.Over the last two decades,intense efforts have been made to identify Treg subsets,Treg differentiation processes,and the molecular signatures and regulators that determine Treg lineage specificity and stability.1–6 Several lines of evidence clearly demonstrate that Foxp3^(+)Tregs do not constitute a homogeneous population,and various subsets of Tregs,such as thymic Tregs(tTregs),in vitro-generated Tregs(iTregs),and peripherally induced Tregs(pTregs),have been identified.5 In addition to Foxp3,epigenetic factors and metabolic processes play key roles in maintaining Treg identity and function,and mediate the switch between effector T cells and Tregs.
出处 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2020年第4期310-312,共3页 中国免疫学杂志(英文版)
基金 supported by ANR-19-CE17-0021(BASIN),Institut National de la Santéet de la Recherche Médicale,Sorbonne Université,and UniversitéParis Descartes,Paris,France.
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