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

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245

New concepts in vascular biology (Part I)

Issue: 2007: 98/2 (Aug) pp. 259-481
Pages: 262-273

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

Jürgen Schymeinsky1, Attila Mócsai2, Barbara Walzog1*

1Dept. of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany; 2Dept. of Physiology, Semmelweis University School of Medicine, Budapest, Hungary


inflammation, signal transduction, integrins, leukocyte trafficking / recruitment


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 com- ponent 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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