Background: C1q is a major molecule of the immune innate system. GAPDH exposed at the surface of cells is associated with the virulence of pathogens. Results: C1q binds GAPDH on human apoptotic and on pneumococcal cells. Conclusion: GAPDH is a C1q ligand. Pneumococcal GAPDH-C1q interaction leads to complement activation. Significance: This might bring new insights into host defense against pathogens.
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