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First published online January 17, 2009


Journal of Cell Science 122, 203e (2009)
© The Company of Biologists Limited
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In this issue

JAM-A – getting neutrophils unstuck


Figure 1

Early in the inflammatory response, neutrophils infiltrate tissues by migrating (extravasating) across the endothelium of blood vessels, then moving chemotactically towards the site of inflammation. The expression of the cell-surface adhesion protein JAM-A in endothelial cells is thought to affect neutrophil extravasation – but does JAM-A expressed in neutrophils also function in infiltration? On page 268, Elisabetta Dejana and colleagues show that it does. The authors have previously demonstrated that, in vitro, JAM-A expression in neutrophils is needed for their efficient directional migration; now, they show that the migration of leukocytes after extravasation is impaired in JAM-A-deficient mice. In activated HL60 neutrophils, they show, JAM-A is internalised into intracellular vesicles that also contain several integrins. Moreover, cell-surface JAM-A co-clusters with β1 integrin in the presence of fibronectin-coated beads or anti-integrin antibodies. Importantly, the internalisation of integrins by neutrophils derived from JAM-A-deficient mice in response to chemotactic signals is impaired, affecting both uropod retraction and cell motility. On the basis of these and other data, the authors propose that JAM-A promotes neutrophil chemotaxis by controlling integrin internalisation and recycling.


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Related articles in JCS:

JAM-A promotes neutrophil chemotaxis by controlling integrin internalization and recycling
Maria Rosaria Cera, Monica Fabbri, Cinzia Molendini, Monica Corada, Fabrizio Orsenigo, Markus Rehberg, Christoph A. Reichel, Fritz Krombach, Ruggero Pardi, and Elisabetta Dejana
JCS 2009 122: 268-277. [Abstract] [Full Text]  




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