ArticleNature immunology2016
Phosphatase PP2A is requisite for the function of regulatory T cells.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
What it found
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Who cites it
145 citing papers in PubMed, 243 citations in OpenAlex.
- PPP2R3C serves as a negative regulator associated with reduced T cell hyperactivation and renal protection in lupus.Clinical and translational medicine · 2026Article
- Restoring B cell intrinsic tolerance to lupus autoimmunity: a rational strategy for lupus treatment.Frontiers in immunology · 2026Review
- Divergent immunometabolic reprogramming in psoriasis and atopic dermatitis: a tale of two inflammatory skin diseases.Frontiers in immunology · 2026Review
- Tumor-immune metabolic tug-of-war: from immune escape to targeting metabolic rewiring in cancer therapy.Frontiers in cell and developmental biology · 2026Review
- AT2R activation reduces M1-type macrophages and promotes tregs accumulation in ischemia-reperfusion-induced acute kidney injury.Frontiers in pharmacology · 2026Article
- Modulation of the tumor microenvironment by the ubiquitin-proteasome system in colorectal cancer.Journal of translational medicine · 2025Review
- Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025Review
- Article
- Decoding the metabolic dialogue in the tumor microenvironment: from immune suppression to precision cancer therapies.Experimental hematology & oncology · 2025Review
- NLRP4 unlocks an NK/macrophages-centered ecosystem to suppress non-small cell lung cancer.Biomarker research · 2025Article
- Gluconolactone restores immune regulation and alleviates skin inflammation in lupus-prone mice and in patients with cutaneous lupus.Science translational medicine · 2025Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- Possible Trace of HTLV-1 Virus in Modulation of Cbl-b, ITCH, and PP2A Suppressor Genes.International journal of molecular and cellular medicine · 2025Article
- Protein serine/threonine phosphatases in tumor microenvironment: a vital player and a promising therapeutic target.Theranostics · 2025Review
- Protein Phosphatase 2A Promotes CD8Research (Washington, D.C.) · 2025Article
- An AMBRA1, ULK1 and PP2A regulatory network regulates cytotoxic T cell differentiation via TFEB activation.Scientific reports · 2024Article
- The influence of metabolic disorders on adaptive immunity.Cellular & molecular immunology · 2024Review
- PPM1G dephosphorylates eIF4E in control of mRNA translation and cell proliferation.Life science alliance · 2024Article
- A combination of protein phosphatase 2A inhibition and checkpoint immunotherapy: a perfect storm.Molecular oncology · 2024Review
- PP2A catalytic subunit alpha is critically required for CD8European journal of immunology · 2024Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Homeostasis of the immune system depends on the proper function of regulatory T cells (T(reg) cells). Compromised suppressive activity of T(reg) cells leads to autoimmune disease and graft rejection and promotes anti-tumor immunity. Here we report a previously unrecognized requirement for the serine-threonine phosphatase PP2A in the function of T(reg) cells. T(reg) cells exhibited high PP2A activity, and T(reg) cell-specific ablation of the PP2A complex resulted in a severe, multi-organ, lymphoproliferative autoimmune disorder. Mass spectrometry revealed that PP2A associated with components of the mTOR metabolic-checkpoint kinase pathway and suppressed the activity of the mTORC1 complex. In the absence of PP2A, T(reg) cells altered their metabolic and cytokine profile and were unable to suppress effector immune responses. Therefore, PP2A is required for the function of T(reg) cells and the prevention of autoimmunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.