{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T00:17:39Z","timestamp":1771460259041,"version":"3.50.1"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":5691,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2000,2]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Galectin-1, an endogenous lectin with immunomodulatory activities, induces selective, Fas-independent apoptosis of activated T cells. The aim of the present study was to evaluate the effect galectin-1 exerts on concanavalin A (Con A)-induced hepatitis, a T-cell-dependent model of liver injury. Con A administration resulted in liver injury, as shown by the increased transaminase plasma levels and liver DNA fragmentation, and caused spleen T-cell activation, which was associated with a strong increment in liver infiltrating T helper cells. Moreover, Con A injection leads to a marked increase in plasma tumor necrosis factor \u03b1 (TNF-\u03b1) and interferon gamma (IFN-\u03b3) levels. Galectin-1 pretreatment dose-dependently prevented both liver injury and T-helper cell liver infiltration induced by Con A. <jats:italic toggle=\"yes\">In vivo<\/jats:italic> and <jats:italic toggle=\"yes\">in vitro<\/jats:italic> experiments indicated that the protective effects of galectin-1 depend on the selective elimination of Con A-activated T cells. In addition, galectin-1 almost completely prevented the Con A-induced increase in plasma TNF-\u03b1 and IFN-\u03b3, an effect that was, at least in part, independent on the elimination of activated T helper cells, because galectin-1 prevented lipopolysaccharide (LPS)-induced release of TNF-\u03b1 and IFN-\u03b3 also from macrophages <jats:italic toggle=\"yes\">in vitro<\/jats:italic>, without affecting their viability. The present study suggests that galectin-1 is potentially useful in the treatment of T-cell-mediated human liver disorders.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.510310220","type":"journal-article","created":{"date-parts":[[2004,7,28]],"date-time":"2004-07-28T07:43:47Z","timestamp":1091000627000},"page":"399-406","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":118,"title":["Galectin-1 exerts immunomodulatory and protective effects on concanavalin a-induced hepatitis in 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