Evidence map›Paper›PMID 31335320›Full record

ArticleJCI insight2019

PPP2R2B hypermethylation causes acquired apoptosis deficiency in systemic autoimmune diseases.

Iris K Madera-Salcedo, Beatriz E Sánchez-Hernández, Yevgeniya Svyryd, Marcela Esquivel-Velázquez, Noé Rodríguez-Rodríguez, María Isabel Trejo-Zambrano, H Benjamín García-González, Gabriela Hernández-Molina, Osvaldo M Mutchinick, Jorge Alcocer-Varela and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
7.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  3. Protein Phosphatase 2A Promotes CD8Research (Washington, D.C.) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Iris K Madera-SalcedoDepartment of Immunology and Rheumatology and.
Beatriz E Sánchez-HernándezDepartment of Genetics, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Yevgeniya SvyrydDepartment of Genetics, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Marcela Esquivel-VelázquezDepartment of Immunology and Rheumatology and.
Noé Rodríguez-RodríguezDepartment of Immunology and Rheumatology and.
María Isabel Trejo-ZambranoDepartment of Immunology and Rheumatology and.
H Benjamín García-GonzálezDepartment of Immunology and Rheumatology and.
Gabriela Hernández-MolinaDepartment of Immunology and Rheumatology and.
Osvaldo M MutchinickDepartment of Genetics, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Jorge Alcocer-VarelaDepartment of Immunology and Rheumatology and.
Florencia RosettiDepartment of Immunology and Rheumatology and.
José C CrispínDepartment of Immunology and Rheumatology and.
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation causes target organ damage in patients with systemic autoimmune diseases. The factors that allow this protracted response are poorly understood. We analyzed the transcriptional regulation of PPP2R2B (B55ß), a molecule necessary for the termination of the immune response, in patients with autoimmune diseases. Altered expression of B55ß conditioned resistance to cytokine withdrawal-induced death (CWID) in patients with autoimmune diseases. The impaired upregulation of B55ß was caused by inflammation-driven hypermethylation of specific cytosines located within a regulatory element of PPP2R2B preventing CTCF binding. This phenotype could be induced in healthy T cells by exposure to TNF-α. Our results reveal a gene whose expression is affected by an acquired defect, through an epigenetic mechanism, in the setting of systemic autoimmunity. Because failure to remove activated T cells through CWID could contribute to autoimmune pathology, this mechanism illustrates a vicious cycle through which autoimmune inflammation contributes to its own perpetuation.

Indexed as

DNA MethylationApoptosisAutoimmune DiseasesCCCTC-Binding FactorCytokinesCytosineGene Expression RegulationHumansInflammationNerve Tissue ProteinsProtein Phosphatase 2T-LymphocytesUp-RegulationCCCTC-Binding FactorCTCF protein, humanCytokinesCytosineNerve Tissue ProteinsPPP2R2B protein, humanProtein Phosphatase 2AutoimmunityImmunologyLupus

Identifiers

PMID31335320
PMCPMC6777834
OpenAlexW2962790437

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.