ArticleCell reports2016
Inflammatory Th17 Cells Express Integrin αvβ3 for Pathogenic Function.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- A cell-intrinsic glucocorticoid biosynthesis and sensing circuit maintains a homeostatic Th17 cell state.Immunity · 2026Article
- Contextualizing TNature reviews. Immunology · 2026Review
- Inhibiting the Secreted RGDKGE Collagen Peptide Selectively Controls CD8The American journal of pathology · 2026Article
- T cell-mediated immunodysregulation in multiple sclerosis: from pathogenic subsets to therapeutic advances.Frontiers in immunology · 2026Review
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- The phenotypic and genetic association between endometriosis and immunological diseases.Human reproduction (Oxford, England) · 2025Article
- Multiple sclerosis: etiology in the context of neurovascular unit and immune system involvement and advancements withFrontiers in immunology · 2025Review
- Basement membranes' role in immune cell recruitment to the central nervous system.Journal of inflammation (London, England) · 2024Article
- Transcription factor TCF1 binds to RORγt and orchestrates a regulatory network that determines homeostatic Th17 cell state.Immunity · 2024Article
- Platelet-derived microparticles adoptively transfer integrin β3 to promote antitumor effect of tumor-infiltrating T cells.Oncoimmunology · 2024Article
- A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS.The Journal of clinical investigation · 2023Article
- Integrin α3 promotes TScience immunology · 2023Article
- The interplay between T helper cells and brain barriers in the pathogenesis of multiple sclerosis.Frontiers in cellular neuroscience · 2023Review
- The immunology of Parkinson's disease.Seminars in immunopathology · 2022Review
- Chemokine-Driven Migration of Pro-Inflammatory CD4Frontiers in immunology · 2022Review
- Endogenous Interleukin-17a Contributes to Normal Spatial Memory Retention but Does Not Affect Early Behavioral or Neuropathological Outcomes after Experimental Traumatic Brain Injury.Neurotrauma reports · 2022Article
- Article
- Asthma and posttraumatic stress disorder (PTSD): Emerging links, potential models and mechanisms.Brain, behavior, and immunity · 2021Review
- The spatio-temporal control of effector T cell migration.Nature reviews. Immunology · 2021Review
- An Overview of Peptide-Based Molecules as Potential Drug Candidates for Multiple Sclerosis.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Interleukin-23 (IL-23) is required for inflammatory Th17 cell function in experimental autoimmune encephalomyelitis (EAE), and IL-23 blockade reduces the number of effector Th17 cells in the CNS. We report that pro-inflammatory Th17 cells express high integrin β3 that is IL-23 dependent. Integrin β3 was not upregulated on all activated T cells; rather, integrin β3 was upregulated along with its functional partner integrin αv on effector Th17 cells and "ex-Th17" cells, and αvβ3(hi) RORγt(+) cells expanded during EAE. Integrin αvβ3 inhibitors ameliorated clinical signs of EAE, and integrin β3 deficiency on CD4(+) T cells alone was sufficient to block EAE induction. Furthermore, integrin-β3-deficient Th17 cells, but not Th1 cells, were impaired in their ability to induce EAE. Integrin β3(-/-) T cells induced smaller demyelinated lesions and showed reduced spread and accumulation within the CNS, corresponding with impaired extracellular-matrix-mediated migration. Hence, integrin β3 is required for Th17 cell-mediated autoimmune CNS inflammation.
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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.