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Published on: February 2, 2024
Neutrophil activation via beta2 integrins (CD11/CD18): molecular mechanisms and clinical implications
Jürgen Schymeinsky1, Attila Mócsai, Barbara Walzog
1Department of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany.
Abstract:
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 beta2 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 beta2 integrins that is required for the control of different PMN functions including adhesion, migration and phagocytosis. The exploration of beta2 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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