{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T15:56:13Z","timestamp":1790006173701,"version":"4.0.1"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,2,5]],"date-time":"2004-02-05T00:00:00Z","timestamp":1075939200000},"content-version":"vor","delay-in-days":4,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To investigate the potential for endothelial cells to operate as superantigen\u2010presenting cells for T cells and the potential for such an interaction to cause endothelial cell activation and injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Class II major histocompatibility complex (MHC)\u2013positive human umbilical vein endothelial cells (HUVECs) were cocultured for 4 hours with purified T cells and the superantigens staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST\u20101). After staining with fluorescence\u2010conjugated monoclonal antibodies, flow cytometric analysis was performed on the HUVECs and T cells to examine V<jats:sub>\u03b2<\/jats:sub>\u2010restricted T cell adherence to the endothelial cell monolayer, V<jats:sub>\u03b2<\/jats:sub>\u2010restricted T cell activation (CD69 up\u2010regulation), surface expression of endothelial cell activation markers, and generation of endothelial microparticles (EMPs).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Coculture of purified T cells with class II MHC\u2013positive HUVECs and either TSST\u20101 or SEB resulted in V<jats:sub>\u03b2<\/jats:sub>\u2010restricted CD69 up\u2010regulation by CD4 and CD8 cells (V<jats:sub>\u03b2<\/jats:sub>2 activation for TSST\u20101; V<jats:sub>\u03b2<\/jats:sub>3, V<jats:sub>\u03b2<\/jats:sub>5.1, and V<jats:sub>\u03b2<\/jats:sub>12 activation for SEB). Additionally, there was CD4 and CD8 T cell V<jats:sub>\u03b2<\/jats:sub>\u2010restricted adherence to the HUVEC monolayer at 4 hours. Expression of intercellular adhesion molecule 1, E\u2010selectin, and vascular cell adhesion molecule 1 was up\u2010regulated on the class II MHC\u2013positive HUVECs following exposure to superantigen in the presence of T cells, and there was increased EMP release from activated HUVECs, which occurred earlier and was of greater magnitude than that observed in response to tumor necrosis factor \u03b1.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Class II MHC\u2013positive endothelial cells operate as competent superantigen\u2010presenting cells for CD4 and CD8 lymphocytes in vitro. Dual signaling between endothelial cells and T cells results in V<jats:sub>\u03b2<\/jats:sub>\u2010restricted activation and adherence to endothelial monolayers and endothelial cell activation and release of EMPs expressing inducible cell adhesion molecules. It is proposed that this mechanism could account in part for the vascular injury associated with superantigen\u2010mediated diseases including Kawasaki disease.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.20021","type":"journal-article","created":{"date-parts":[[2004,2,9]],"date-time":"2004-02-09T18:29:18Z","timestamp":1076351358000},"page":"589-597","source":"Crossref","is-referenced-by-count":41,"title":["V<sub>\u03b2<\/sub>\u2010restricted T cell adherence to endothelial cells: A mechanism for superantigen\u2010dependent vascular injury"],"prefix":"10.1002","volume":"50","author":[{"given":"P. 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