CD177 modulates human neutrophil migration through activation-mediated integrin and chemoreceptor regulation

Ming Bai(Brigham and Women's Hospital), Ricardo Grieshaber‐Bouyer(Brigham and Women's Hospital), Junxia Wang(Brigham and Women's Hospital), Angela B. Schmider(Massachusetts General Hospital), Zachary Wilson(Providence College), Liling Zeng(Novartis (United States)), Olha Halyabar(Brigham and Women's Hospital), Matthew D. Godin(Massachusetts General Hospital), Hung N. Nguyen(Brigham and Women's Hospital), Anaïs Levescot(Brigham and Women's Hospital), Pierre Cunin(Brigham and Women's Hospital), Craig T. Lefort(Providence College), Roy J. Soberman(Massachusetts General Hospital), Peter A. Nigrović(Brigham and Women's Hospital)
Blood
August 15, 2017
10.1182/blood-2017-03-768507
Cited by 193Open Access
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Abstract

neutrophils, an effect mediated through immobilization and cellular spreading on the transwell membrane. Correspondingly, CD177 ligation enhanced its interaction with β2 integrins, as revealed by fluorescence lifetime imaging microscopy, leading to integrin-mediated phosphorylation of Src and extracellular signal-regulated kinase (ERK). CD177-driven cell activation enhanced surface β2 integrin expression and affinity, impaired internalization of integrin attachments, and resulted in ERK-mediated attenuation of chemokine signaling. We conclude that CD177 signals in a β2 integrin-dependent manner to orchestrate a set of activation-mediated mechanisms that impair human neutrophil migration.

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