ArticleProceedings of the National Academy of Sciences of the United States of America2011
Induction of PP2A Bβ, a regulator of IL-2 deprivation-induced T-cell apoptosis, is deficient in systemic lupus erythematosus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 51 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
- Capicua mediates interleukin-2 withdrawal-induced death of activated CD8Cell insight · 2026Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- Protein Phosphatase 2A Promotes CD8Research (Washington, D.C.) · 2025Article
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- The PP2A regulatory subunit PPP2R2A controls NADCell reports · 2024Article
- Rapid anti-myeloma activity by T cells expressing an anti-BCMA CAR with a human heavy-chain-only antigen-binding domain.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Update of Potential Biomarkers in Risk Prediction and Monitoring of Atherosclerosis in Systemic Lupus Erythematosus to Prevent Cardiovascular Disease.Biomedicines · 2023Review
- The star target in SLE: IL-17.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- miR21 modulates the Hippo signaling pathway via interference with PP2A Bβ to inhibit trophoblast invasion and cause preeclampsia.Molecular therapy. Nucleic acids · 2022Article
- PPP2R2D Suppresses Effector T Cell Exhaustion and Regulatory T Cell Expansion and Inhibits Tumor Growth in Melanoma.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy.Signal transduction and targeted therapy · 2022Review
- Regulation of activated T cell survival in rheumatic autoimmune diseases.Nature reviews. Rheumatology · 2022Review
- [Systemic lupus erythematosus-are children small adults?]Zeitschrift fur Rheumatologie · 2022Review
- The Regulatory Subunit PPP2R2A of PP2A Enhances Th1 and Th17 Differentiation through Activation of the GEF-H1/RhoA/ROCK Signaling Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy.Current opinion in rheumatology · 2021Review
- Systemic Lupus Erythematosus in Children and Young People.Current rheumatology reports · 2021Review
- Protein phosphatase 2A B55β limits CD8+ T cell lifespan following cytokine withdrawal.The Journal of clinical investigation · 2020Article
- PPP2R2D suppresses IL-2 production and Treg function.JCI insight · 2020Article
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4 authors at 2 institutions in 1 country.
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Abstract
The activity and substrate specificity of the ubiquitously expressed phosphatase PP2A is determined by the type of regulatory (B) subunit that couples to the catalytic/scaffold core of the enzyme. We determined that the Bβ subunit (PPP2R2B) is expressed in resting T cells, its transcription is down-regulated during T-cell activation, and up-regulated in conditions of low IL-2. Specifically, high levels of PP2A Bβ were produced during IL-2 deprivation-induced apoptosis, whereas Fas ligation had no effect. Forced expression of the Bβ subunit in primary human T cells was sufficient to induce apoptosis, whereas silencing using siRNA protected activated T cells from IL-2 withdrawal-induced cell death. Because T-cell apoptosis is known to be altered in T cells from patients with systemic lupus erythematosus, we analyzed the regulation of PP2A Bβ in this autoimmune disease. We found that levels of PP2A Bβ did not increase upon IL-2 deprivation in 50% of the patients. Remarkably, this defect was accompanied by resistance to apoptosis. Importantly, kinetics of cell death were normal in cells of patients that up-regulated PP2A Bβ in a normal manner. We have identified a unique role for the phosphatase PP2A, particularly the holoenzyme formed by PP2A Bβ. Bβ appears to trigger apoptosis of T cells in the absence of IL-2 and probably contributes to the termination of a no-longer-needed immune response. We propose that defective production of PP2A Bβ upon IL-2 deprivation results in apoptosis resistance and longer survival of autoreactive T cells, in a subset of SLE patients.
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