Thromb Haemost 2007; 98(02): 262-273
DOI: 10.1160/TH07-02-0156
Theme Issue Article
Schattauer GmbH

Neutrophil activation via β2 integrins (CD11/CD18): Molecular mechanisms and clinical implications

Jürgen Schymeinsky
1   Dept. of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany
,
Attila Mócsai
2   Dept. of Physiology, Semmelweis University School of Medicine, Budapest, Hungary
,
Barbara Walzog
1   Dept. of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany
1   Dept. of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany
› Author Affiliations
Further Information

Publication History

Received 28 February 2007

Accepted after revision 03 May 2007

Publication Date:
28 November 2017 (online)

Summary

Polymorphonuclear neutrophils (PMN) are key components of the innate immunity and their efficient recruitment to the sites of lesion is a prerequisite for acute inflammation. Signaling via adhesion molecules of the β2 integrin family (CD11/CD18) plays an essential role for PMN recruitment and activation during inflammation. In this review, we will focus on the non-receptor tyrosine kinase Syk, an important downstream signaling component of β2 integrins that is required for the control of different PMN functions including adhesion,migration and phagocytosis. The exploration of β2 integrin-mediated Syk activation provided not only novel insights into the control of PMN functions but also led to the identification of Syk as a new molecular target for therapeutic intervention during inflammatory diseases.

 
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