ArticleJournal of leukocyte biology2025
Piezo1 restrains proinflammatory response but is essential in T-cell-mediated immunopathology.
Article in Journal of leukocyte biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
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Who cites it
9 citing papers in PubMed.
- The mechano-immunological landscape in the tumor microenvironment: From mechanical sensing to a new therapeutic paradigm.Materials today. Bio · 2026Review
- Piezo1 in the central nervous system: decoding the mechanical signature of neuroinflammation.Journal of neuroinflammation · 2026Review
- The Dual Role of Piezo1 in Cancer: Mechanotransduction, Microenvironment Remodelling, and Therapeutic Opportunities.Drug design, development and therapy · 2026Review
- The role of ECM-PIEZO1-axis-mediated mechanosensation in the central nervous system.Frontiers in neurology · 2026Review
- The role of Piezo1 in immune cells and pregnancy.Frontiers in immunology · 2026Review
- Piezo1 in immune cells: from mechanosensation to immunoregulation.Frontiers in immunology · 2026Review
- Piezo1 Mechanosensor Expression in Rare Hematopoietic Cells Controls Systemic Inflammatory Response in Mice.Cells · 2025Article
- Piezo1 in heart failure: A new perspective from cytomechanical sensing to diverse cellular pathways.Molecular biology reports · 2025Review
- Mechanical interactions impact the functions of immune cells and their application in immunoengineering.Advanced therapeutics · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Piezo1 is a mechanosensitive, nonselective Ca2+ channel that is broadly expressed in CD4+ T cells. Using lineage-specific Piezo1 knockout mice (Piezo1cKO), we show that loss of Piezo1 in CD4+ T cells significantly increased IFNγ and IL-17 production in vitro under TH1 and TH17 polarizing conditions, respectively. Despite their intrinsic proinflammatory phenotype, Piezo1cKO T cells are incapable of establishing disease in vivo in 3 separate adoptive transfer T-cell-mediated inflammatory mouse models, including experimental autoimmune encephalomyelitis, inflammatory bowel disease, and graft-vs-host disease. These phenomena coincided with a decreased effector memory (CD44hiCD62Llo) CD4+ T-cell pool derived from donor Piezo1cKO T cells, an observation related to intrinsic T-cell fitness, as a cotransfer inflammatory bowel disease mouse model revealed a deficiency in the CD4+ effector memory population derived only from the naive Piezo1cKO but a not coinfused Piezo1WT CD4+ T-cell source. Taken together, our results support Piezo1 as restraining proinflammatory T-cell differentiation while contributing to the generation and persistence of the effector memory pool during CD4+ T-cell-mediated immunopathology.
Indexed as
Identifiers
What Socratic holds
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.