ArticleThe Journal of experimental medicine2004
CD43 regulation of T cell activation is not through steric inhibition of T cell-APC interactions but through an intracellular mechanism.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 47 citations in OpenAlex.
- Surfaceome CRISPR activation screening uncovers ligands regulating tumor sensitivity to NK cell killing.Nature communications · 2026Article
- Studying Macromolecular Composition in Cell-Cell Interfaces Using 3D Membrane Reconstitution Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Wiskott-Aldrich syndrome and X-linked thrombocytopenia: a review of the clinical and immunological spectrum with a case presentation highlighting glomerulonephritis.Frontiers in pediatrics · 2026Review
- Review
- Targeting CD43 optimizes cancer immunotherapy through reinvigorating antitumor immune response in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- SARS-CoV-2 spike protein induces a differential monocyte activation that may contribute to age bias in COVID-19 severity.Scientific reports · 2022Article
- ERM Proteins at the Crossroad of Leukocyte Polarization, Migration and Intercellular Adhesion.International journal of molecular sciences · 2020Review
- CD43 sialoglycoprotein modulates cardiac inflammation and murine susceptibility to Trypanosoma cruzi infection.Scientific reports · 2019Article
- Engagement of distinct epitopes on CD43 induces different co-stimulatory pathways in human T cells.Immunology · 2016Article
- Comparative Anatomy of Phagocytic and Immunological Synapses.Frontiers in immunology · 2016Review
- CD43-mediated IFN-γ production by CD8+ T cells promotes abdominal aortic aneurysm in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Ex vivo enzymatic treatment of aged CD4 T cells restores cognate T cell helper function and enhances antibody production in mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- T cells modulate glycans on CD43 and CD45 during development and activation, signal regulation, and survival.Annals of the New York Academy of Sciences · 2012Review
- Role of O-glycosylation and expression of CD43 and CD45 on the surfaces of effector T cells in human T cell leukemia virus type 1 cell-to-cell infection.Journal of virology · 2012Article
- Development of IgA nephropathy-like glomerulonephritis associated with Wiskott-Aldrich syndrome protein deficiency.Clinical immunology (Orlando, Fla.) · 2012Article
- CD43 interaction with ezrin-radixin-moesin (ERM) proteins regulates T-cell trafficking and CD43 phosphorylation.Molecular biology of the cell · 2011Article
- Age-related defects in the cytoskeleton signaling pathways of CD4 T cells.Ageing research reviews · 2011Review
- CD43 regulates Th2 differentiation and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- CD43 signals induce Type One lineage commitment of human CD4+ T cells.BMC immunology · 2007Article
- Age-related defects in moesin/ezrin cytoskeletal signals in mouse CD4 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
CD43 is a large heavily glycosylated protein highly expressed on T cells and actively excluded from the immunological synapse through interactions with ezrin-radixin-moesin proteins. Due to its size and charge, it has been proposed that the CD43 ectodomain acts as a physical barrier to T cell-APC interactions. We have addressed this hypothesis by studying the effect of reconstituting CD43 mutants into the hyperproliferative CD43(-/-) T cells. Reintroduction of full-length CD43 reversed the CD43(-/-) T cell hyperproliferation. Interestingly, despite the lack of exclusion from the interaction site, a mutant containing the CD43 ectodomain on a glycosylphosphatidylinositol linkage was ineffective. Additionally, T cell-APC conjugate formation was not affected by this ectodomain-only construct. In contrast, CD43(-/-) T cell hyperproliferation was reversed by an intracellular-only CD43 fused to the small ectodomain of hCD16. Mutation of this intracellular-only CD43 such that it could not move from the T cell-APC contact site had no further affect on proliferation than the moveable CD43 but did dramatically reduce interleukin-2 production. Thus, the exclusion of the CD43 intracellular region from the immunological synapse is required for CD43 regulation of interleukin-2 production, but the presence of the cytoplasmic tail, independent of its location, is sufficient to reverse CD43(-/-) T cell hyperproliferation.
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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.