Figure (IMAGE)

Osaka University

Figure

Caption

Graphical scheme of this study. Under healthy conditions, the interaction between endothelial plexin B2 ligand and neutrophil cells surface SEMA4D receptor inhibits Rac1 activation and negatively regulates the generation of ROS and NET formation. By contrast, in AAV patients, neutrophil surface SEMA4D is shed by ADAM17. Soluble SEMA4D had pro-inflammatory functions on endothelial cells. In addition, alteration of the SEMA4D-plexin B2 interaction results in aberrant activation of neutrophils, and this dichotomous effect is involved in the pathogenesis of AAV.

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Osaka University

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