Fig. 1
From: Dectin-1/Syk signaling triggers neuroinflammation after ischemic stroke in mice
Working model for the present study. Injured cells release damage-associated molecular patterns and activate innate immunity via receptors, such as Dectin-1. Then, the ligand phosphorylates ITAM and recruits the downstream kinase Syk, which phosphorylates Syk and drives inflammatory cascades and cytokine production. The Dectin-1 antagonist laminarin and Syk inhibitor piceatannol can decrease the release of the inflammatory cytokines induced by ischemia. Dectin-1/Syk signaling appears to play a vital role in the inflammatory response after a stroke