ArticleIn vivo (Athens, Greece)
Blocking of Type 1 Angiotensin II Receptor Inhibits T-lymphocyte Activation and IL-2 Production.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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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.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Single-Cell Transcriptomics Reveals Immune Modulation by Telmisartan in Colorectal Cancer.Cells · 2026Article
- Immunomodulatory Effects of RAAS Inhibitors: Beyond Hypertension and Heart Failure.Biomedicines · 2025Review
- Angiotensin II Type I Receptor (AT1R): The Gate towards COVID-19-Associated Diseases.Molecules (Basel, Switzerland) · 2022Review
- Immunomodulatory Activity of the Most Commonly Used Antihypertensive Drugs-Angiotensin Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers.International journal of molecular sciences · 2022Review
- Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimNovel information on the role of endogenous compounds in regulating physiological and pathological process are of interest, as it may lead to the development of better strategies for disease management. The role of angiotensin II and the signaling of type 1 angiotensin II receptor (AGT1R) in T-lymphocyte activation and interleukin-2 (IL-2) production are largely unknown. MATERIALS AND
methodsJurkat T-cells were treated with AGT1R inhibitor candesartan and stimulated with phorbol myristate acetate (PMA) and ionomycin. T-Cell activation, associated cytokine production and levels of signaling proteins were evaluated by flow cytometry and western blot analysis.
resultsCandesartan significantly suppressed PMA and ionomycin-induced CD25 expression and IL-2 production. Regarding the molecular mechanism involved, we showed that such suppressive effects of blocking of AGT1R by candesartan resulted in the significant inhibition of ERK activation in PMA-stimulated Jurkat T-cells. The effect of ERK inhibition on T-cell activation was further confirmed. Treatment with FR180204, a specific ERK inhibitor, reduced T-cell activation and IL-2 secretion.
conclusionAGT1R signaling is essential for T-cell activation and IL-2 production, and the inhibition of this pathway suppressed T-cell activation via an ERK-dependent mechanism.
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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 Socratic graph.