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c-Abl Kinase Is Required for β₂ Integrin-Mediated Neutrophil Adhesion¹

Lingling Cui^*, Cuixia Chen^*,, Ting Xu^*, Juechao Zhang^*, Xin Shang^*, Jixian Luo^*, Liang Chen^*, Xueqing Ba^* and Xianlu Zeng^2,*

^* Institute of Genetics and Cytology, Northeast Normal University, Changchun, People’s Republic of China; and Center for Bioengineering and Biotechnology, China University of Petroleum (East China), Qingdao, People’s Republic of China

Integrin regulation in neutrophil adhesion is essential for innate immune response. c-Abl kinase is a nonreceptor tyrosine kinase and is critical for signaling transduction from various receptors in leukocytes. Using neutrophils and dHL-60 (neutrophil-like differentiation of HL-60) cells, we show that c-Abl kinase is activated by β₂ integrin engagement and is required for β₂ integrin-dependent neutrophil sustained adhesion and spreading. The expression of β₂ integrin on neutrophils induced by TNF- is not affected by c-Abl kinase inhibitor STI571, suggesting that c-Abl kinase is not involved in TNF--induced integrin activation. The recruitment of c-Abl kinase to β₂ integrin is dependent on talin head domain, which constitutively interacts with β₂ integrin cytoplasmic domain. After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav. The SH3 domain of c-Abl kinase is involved in its interaction with talin and Vav. Thus, c-Abl kinase plays an essential role in the activation of Vav induced by β₂ integrin ligation and in regulating neutrophil-sustained adhesion and spreading.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the National Natural Science Foundation of China (30570927, 30570928), National Basic Research Program of China (2005CB522404), and Training Fund of Northeast Normal University’s Scientific Innovation Project (NENU-STC 7011).

² Address correspondence and reprint requests to Dr. Xianlu Zeng, Institute of Genetics and Cytology, Northeast Normal University, 5268 Renmin Street, Changchun 130024, People’s Republic of China. E-mail address: zengx779{at}nenu.edu.cn

³ Abbreviations used in this paper: SH, Src homology; CTD, C-terminal domain; dHL-60, neutrophil-like differentiation of HL-60.

⁴ The online version of this article contains supplemental material.

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The JI 2009 182: 2555-2556. [Full Text]