{ "labelLang" : "hun", "responseDate" : "2024-03-28 11:52", "content" : { "otype" : "JournalArticle", "mtid" : 3190069, "status" : "VALIDATED", "published" : true, "comment" : "Institute of Genetics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary \n Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Szeged, 6725, Hungary \n Cited By :1 \n Export Date: 18 September 2019 \n CODEN: LUPUE \n Correspondence Address: Kovács, L.; Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Hungary; email: kovacs.laszlo@med.u-szeged.hu \n Chemicals/CAS: galectin 1, 258495-34-0; ganglioside GM1, 37758-47-7; phosphatidylinositol 3 kinase, 115926-52-8; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, 210488-47-4; protein kinase Lck, 114051-78-4; protein kinase Syk, 138674-26-7; protein kinase 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Its most important effects are the inhibition of the differentiation and cytokine production of Th1 and Th17 cells, and the induction of apoptosis of activated T-cells. Galectin-1 has been identified as a key molecule in antitumor immune surveillance, and data are accumulating about the pathogenic role of its deficiency, and the beneficial effects of its administration in various autoimmune disease models. Initial animal and human studies strongly suggest deficiencies in both galectin-1 production and responsiveness in systemic lupus erythematosus (SLE) T-cells. Since lupus features widespread abnormalities in T-cell activation, differentiation and viability, in this review the authors wished to highlight potential points in T-cell signalling processes that may be influenced by galectin-1. These points include GM-1 ganglioside-mediated lipid raft aggregation, early activation signalling steps involving p56Lck, the exchange of the CD3 zeta-ZAP-70 to the FcRgamma-Syk pathway, defective mitogen-activated protein kinase pathway activation, impaired regulatory T-cell function, the failure to suppress the activity of interleukin 17 (IL-17) producing T-cells, and decreased suppression of the PI3K-mTOR pathway by phosphatase and tensin homolog (PTEN). 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