Figure 4.

Summary of galectins against influenza A virus infection. Influenza A virus (IAV) infection triggered the induction and secretion of galectin-1 (Gal-1), galectin-3 (Gal-3), and galectin-9 (Gal-9). Secreted Gal-1 could bind to HA glycoprotein of IAVs and further blocking IAV interaction with sialic acid receptors expressed on the cells. IAV infection upregulated endogenous Gal-3, which could induce NLRP3 inflammasome activation, as well as IL-1β secretion, to result in inflammation occurrence. The secreted Gal-9 could interact with Tim-3 expressing cells. Gal-9/Tim-3 interaction triggered Tim-3 downstream signaling and induced apoptosis.