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. Author manuscript; available in PMC: 2010 Sep 29.
Published in final edited form as: Circulation. 2009 Sep 14;120(13):1255–1265. doi: 10.1161/CIRCULATIONAHA.109.873695

Figure 5. Model of Mac-1 mediated inflammation induced thrombosis in TGN.

Figure 5

Anti-GBM antibody in combination with LPS results in in situ immune complex formation and endothelial cell activation. This triggers neutrophil recruitment through Mac-1, which further promotes endothelial cell activation. Engagement of Mac-1 results in neutrophil elastase release, which enhances neutrophil influx. Recruited neutrophils promote platelet accumulation. Platelets initially protect the vessel wall from neutrophil mediated sequelae (-). However, subsequent interaction of Mac-1 on recruited neutrophils with GpIbα on platelets triggers thrombosis (+) that is responsible for vessel occlusion and organ damage.