Related Experiment Video
Updated: Aug 7, 2026

An Endothelial Planar Cell Model for Imaging Immunological Synapse Dynamics
Published on: December 24, 2015
Endothelial nitric oxide synthase regulates T cell receptor signaling at the immunological synapse
Sales Ibiza1, Víctor M Víctor1, Irene Boscá1
1Unidad Mixta: Centro Nacional de Investigaciones Cardiovasculares (CNIC), Universitat de Valencia, Avenida Blasco Ibáñez 15-17, E-46010 Valencia, Spain.
Abstract:
The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence of CD3 at the T cell-APC contact site, which was accompanied by increased phosphorylation of CD3zeta chain, ZAP-70, and extracellular signal-regulated kinases and increased IFN-gamma synthesis, but reduced production of IL-2. Therefore, eNOS-derived NO selectively potentiates T cell receptor signaling to antigen at the immunological synapse.
More Related Videos
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Nitric Oxide Signaling Pathway
T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
Regulation of Angiogenesis and Blood Supply
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...

