ArticleThe Journal of experimental medicine1998
Adenosine diphosphate (ADP)-ribosylation of the guanosine triphosphatase (GTPase) rho in resting peripheral blood human T lymphocytes results in pseudopodial extension and the inhibition of T cell activation.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 33 citations in OpenAlex.
- Effects of the Rho/Rho-Kinase Pathway on Perfusion Pressure in the Isolated-Perfused Rat Hind Limb Vascular Bed.Balkan medical journal · 2021Article
- Role of Macrophages and RhoA Pathway in Atherosclerosis.International journal of molecular sciences · 2020Review
- Autophagy deficiency promotes triple-negative breast cancer resistance to T cell-mediated cytotoxicity by blocking tenascin-C degradation.Nature communications · 2020Article
- The role of tenascin-C in tissue injury and tumorigenesis.Journal of cell communication and signaling · 2009Article
- Rho kinase: an important mediator of atherosclerosis and vascular disease.Current pharmaceutical design · 2009Review
- Small GTP-binding protein Rho-mediated signaling promotes proliferation of rheumatoid synovial fibroblasts.Arthritis research & therapy · 2005Article
- Vav GEFs are required for beta2 integrin-dependent functions of neutrophils.The Journal of cell biology · 2004Article
- Control of T lymphocyte morphology by the GTPase Rho.BMC cell biology · 2003Article
- Cytohesin-1 regulates beta-2 integrin-mediated adhesion through both ARF-GEF function and interaction with LFA-1.The EMBO journal · 2000Article
- Modulation of HIV-1 replication by a novel RhoA effector activity.Journal of immunology (Baltimore, Md. : 1950) · 2000Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Scrape loading Clostridium botulinum C3 exoenzyme into primary peripheral blood human T lymphocytes (PB T cells) efficiently adenosine diphosphate (ADP)-ribosylates and thus inactivates the guanosine triphosphatase (GTPase) Rho. Basal adhesion of PB T cells to the beta1 integrin substrate fibronectin (Fn) was not inhibited by inactivation of Rho, nor was upregulation of adhesion using phorbol myristate acetate (PMA; 10 ng/ml) or Mn++ (1 mM) affected. Whereas untreated PB T cells adherent to Fn remain spherical, C3-treated PB T cells extend F-actin-containing pseudopodia. Inactivation of Rho delayed the kinetics of PMA-dependent PB T cell homotypic aggregation, a process involving integrin alphaLbeta2. Although C3 treatment of PB T cells did not prevent adhesion to the beta1 integrin substrate Fn, it did inhibit beta1 integrin/CD3-mediated costimulation of proliferation. Analysis of intracellular cytokine production at the single cell level demonstrated that ADP-ribosylation of Rho inhibited beta1 integrin/ CD3 and CD28/CD3 costimulation of IL-2 production within 6 h of activation. Strikingly, IL-2 production induced by PMA and ionomycin was unaffected by C3 treatment. Thus, the GTPase Rho is a novel regulator of T lymphocyte cytoarchitecture, and functional Rho is required for very early events regulating costimulation of IL-2 production in PB T cells.
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