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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 \u03b6-ZAP-70 to the FcR\u03b3-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). These findings place galectin-1 into the group of potential pathogenic molecules in SLE.<\/jats:p>","DOI":"10.1177\/0961203316686846","type":"journal-article","created":{"date-parts":[[2017,1,21]],"date-time":"2017-01-21T12:10:49Z","timestamp":1485000649000},"page":"339-347","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function"],"prefix":"10.1177","volume":"26","author":[{"given":"\u00c1","family":"Hornung","sequence":"first","affiliation":[{"name":"Institute of Genetics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary"},{"name":"Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Gy\u00f6rgyi Health Centre, Szeged, 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