Lymphocytes rolling on high endothelial venules stop abruptly in response to chemokines presented by endothelial cells, according to a report published online in Nature Immunology today (April 18). The finding challenges previous notions of the mechanism of leukocyte arrest.

Ronen Alon, of the Weizmann Institute of Science, Rehovot, Israel, and colleagues found that chemokines trigger instantaneous extension of the LFA-1 integrin—an adhesion molecule that can change between an inactive, bent conformation and an active, extended conformation. "The chemokine-mediated extension generates an intermediate affinity form of LFA-1, which brings the integrin head piece into close proximity with the adhesion molecule ICAM-1," Alon told The Scientist. "Then, ICAM-1 triggers the conversion to high affinity."

The physiological and biochemical data that the authors present argues for an integrin activation that happens in 0.1 to 0.5 seconds, resulting in a sudden arrest. "For a long time, it was believed that cells...

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