ArticleThe Journal of clinical investigation2023
Foxp3-mediated blockage of ryanodine receptor 2 underlies contact-based suppression by regulatory T cells.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
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- Unveiling the role of TAM-derived extracellular vesicles in glioma progression through Treg polarization and immune suppression.Oncogene · 2025Article
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- Role of type 2 ryanodine receptor stabilisation in autoimmune cell modulation.Advances in rheumatology (London, England) · 2024Article
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- The role of microRNA-142a in Toxoplasma gondii infection-induced downregulation of Foxp3: implications for adverse pregnancy outcomes.BMC infectious diseases · 2024Article
- Pathophysiology and clinical relevance of atrial myopathy.Basic research in cardiology · 2024Review
- Strengthening bonds via RyR2 inhibition helps immune suppression.The Journal of clinical investigation · 2023Article
- Sustained store-operated calcium entry utilizing activated chromatin state leads to instability in iTregs.eLife · 2023Article
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26 authors at 5 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
The suppression mechanism of Tregs remains an intensely investigated topic. As our focus has shifted toward a model centered on indirect inhibition of DCs, a universally applicable effector mechanism controlled by the transcription factor forkhead box P3 (Foxp3) expression has not been found. Here, we report that Foxp3 blocked the transcription of ER Ca2+-release channel ryanodine receptor 2 (RyR2). Reduced RyR2 shut down basal Ca2+ oscillation in Tregs, which reduced m-calpain activities that are needed for T cells to disengage from DCs, suggesting a persistent blockage of DC antigen presentation. RyR2 deficiency rendered the CD4+ T cell pool immune suppressive and caused it to behave in the same manner as Foxp3+ Tregs in viral infection, asthma, hypersensitivity, colitis, and tumor development. In the absence of Foxp3, Ryr2-deficient CD4+ T cells rescued the systemic autoimmunity associated with scurfy mice. Therefore, Foxp3-mediated Ca2+ signaling inhibition may be a central effector mechanism of Treg immune suppression.
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