This study was supported financially by grant # IPI-195 from Pasteur Institute of Iran. The authors would like to thank Dr. Anis Jafary and Dr. Fariborz Bahrami for their carefully review of the manuscript and other colleagues in Pasteur Institute of Iran, Mrs. M. Zaman-Vaziri for her technical assistance in culturing of the parasites; and Mr. A.H. Javadi for his administrative help. The authors declare that they have no conflict of interest. “
“The endothelial cell adhesion molecule, CD146, is expressed on ≈ 2% of normal circulating T cells, correlating with T cell activation, endothelial interactions and T helper type 17 (Th17) effector functions. In this study, we

have characterized CD146 expression

in circulating T cells from healthy controls www.selleckchem.com/products/Fulvestrant.html and patients with stable, well-controlled autoimmune connective tissue diseases (CTDs). In vitro, anti-CD3/anti-CD28 stimulation induced CD146 expression in both CD4 and CD8 T cells. In healthy controls and CTD patients, CD146 was associated with expression of recent and chronic activation markers (CD25+, OX-40+, CD69+, CD27–) and was confined to CD45RO+/RA–/CD28+ populations within the CD4 subset. Except for CD69, these markers were not associated with CD146 in the CD8 subset. Surprisingly, most CTD patients exhibited no T cell this website hyperactivation ex vivo. In five of five patients with secondary Sjögren’s syndrome circulating T cells appeared activated despite therapy, and CD146 up-regulation, associated with activation markers, was observed both on CD4 and CD8 T cells. There was no association between CD146 and putative pro-atherogenic T cell subsets. In conclusion, the relationship of CD146 expression to T cell activation differs between T cell subsets in healthy subjects and correlates with systemic hyperactivity, selleck where present, in patients with CTDs, as exemplified by the patients with secondary Sjögren’s syndrome in this study. CD146/melanoma cell adhesion molecule (MelCAM) is an immunoglobulin superfamily glycoprotein expressed at

endothelial tight junctions on vascular smooth muscle cells and trophoblast cells, and variably on malignant melanoma cells [1, 2]. Human T cells induce CD146 expression after mitogen stimulation [3]. In vivo, CD146+ T cells are enriched in delayed-type hypersensitivity lesions [3]; cerebrospinal fluid in multiple sclerosis [4]; and synovial effusions, tissue and blood in inflammatory arthritis [3, 5] (C. Wu, R. Busch, J.S.H. Gaston, unpublished). CD146 is present on 1–2% of circulating T, B and natural killer (NK) cells of healthy humans [6, 7], whereas murine CD146 is expressed on neutrophils and NK cells [8]. In these studies, CD146 on CD4+ cells was associated with activation and memory markers, increased adhesion to cytokine-activated endothelia and T helper type 17 (Th17) (and Th1) effector functions.