Journal
CELL REPORTS
Volume 10, Issue 9, Pages 1626-1638Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.02.012
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Funding
- Swedish Research Council
- A.E. Berger Foundation
- Bergvall Foundation
- Crafoord Foundation
- G. & J. Koch Foundation
- Gyllenstiernska Krapperup Foundation
- Karolinska Institute research grants
- Lars Hierta Memorial Foundation
- Proyecto de Excelencia from Junta de Andalucia [CTS-6494]
- Royal Physiographic Society
- Royal Physiographic Society in Lund Foundation
- Spanish Ministerio de Ciencia y Tecnologia [SAF2009-13778]
- Stohnes Foundation
- Swedish Cancer Society
- Swedish Research Council [2012-2229]
- Swedish Parkinson Foundation
- Swedish Strategic Research Area MultiPark at Lund University
- Swedish National Stroke Foundation
- Wiberg Foundation
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Inflammatory 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.
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