Burguillos García, Miguel ÁngelSvensson, MartinaSchulte, TimBoza Serrano, AntonioGarcía Quintanilla, AlbertoKavanagh, Edel T.Santiago Pavón, MartinianoViceconte, NikenzaOliva Martín, María JoséOsman, Ahmed MohamedSalomonsson, EmmaAmar, LahouariPersson, AnnetteBlomgren, KlasAchour, AdnaneEnglund, ElisabetLeffler, HakonVenero Recio, José LuisJoseph, BertrandDeierborg, Tomas2016-05-242016-05-242015Burguillos García, M.Á., Svensson, M., Schulte, T., Boza Serrano, A., García Quintanilla, A., Kavanagh, E.T.,...,Deierborg, T. (2015). Microglia-secreted galectin-3 acts as a toll-like receptor 4 ligand and contributes to microglial activation. Cell Reports, 10 (9), 1626-1639.2211-1247http://hdl.handle.net/11441/41543Inflammatory response induced by microglia plays a critical role in the demise of neuronal populations in neuroinflammatory diseases. Although the role of toll-like receptor 4 (TLR4) in microglia’s inflammatory response is fully acknowledged, little is known about endogenous ligands that trigger TLR4 activation. Here, we report that galectin-3 (Gal3) released by microglia acts as an endogenous paracrine TLR4 ligand. Gal3-TLR4 interaction was further confirmed in a murine neuroinflammatory model (intranigral lipopolysaccharide [LPS] injection) and in human stroke subjects. Depletion of Gal3 exerted neuroprotective and anti-inflammatory effects following global brain ischemia and in the neuroinflammatory LPS model. These results suggest that Gal3-dependent- TLR4 activation could contribute to sustained microglia activation, prolonging the inflammatory response in the brainapplication/pdfengAttribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccess