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dc.contributor.authorBurguillos, MA
dc.contributor.authorSvensson, M
dc.contributor.authorSchulte, T
dc.contributor.authorBoza-Serrano, A
dc.contributor.authorGarcia-Quintanilla, A
dc.contributor.authorKavanagh, E
dc.contributor.authorSantiago, M
dc.contributor.authorViceconte, N
dc.contributor.authorOliva-Martin, MJ
dc.contributor.authorOsman, AM
dc.contributor.authorSalomonsson, E
dc.contributor.authorAmar, L
dc.contributor.authorPersson, A
dc.contributor.authorBlomgren, K
dc.contributor.authorAchour, A
dc.contributor.authorEnglund, E
dc.contributor.authorLeffler, H
dc.contributor.authorVenero, JL
dc.contributor.authorJoseph, B
dc.contributor.authorDeierborg, T
dc.description.abstractInflammatory 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 brain.
dc.titleMicroglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation.
dc.relation.isPartOfCell Rep

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