Immune cells traveling in the bloodstream can abruptly stop at signs of trouble according to new research in the May issue of Nature Immunology. By responding to chemical signals deposited on blood vessel walls, immune cells rapidly deploy specialized attachment molecules that latch onto cells lining the blood vessel, allowing their exit into the damaged tissues.
Previously, exit from the bloodstream was thought to be a gradual process that required braking before exiting at the site of final immune cell arrest. Ronen Alon and colleagues dispel this notion by showing immune cells can immediately stop upon encountering immobilized chemokines ? which act as traffic signals for these cells. Chemokines trigger extension of surface adhesion molecules called LFA-1. The process of extending these molecules unveils a specialized region that acts as a grappling hook for receptors expressed on blood vessel cells. Importantly, it is the immobilized form of chemokine that mediates this signal. The new work explains how immune cells that act as first responders can quickly arrive at scenes of damage.
Ronen Alon (Weizmann Institute of Science, Rehovot, Israel)
Also available online.
(C) Nature Immunology press release.
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