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Constraining neutrophil damage

Nature Immunology

June 30, 2008

The way in which neutrophils ? the immune system’s ‘first responders’ ? migrate into target tissues is reported online this week in Nature Immunology.

Neutrophils are the ‘look-out’ white blood cells that can exit the bloodstream at the first sign of infection and travel to its source. Here they can release their payload of noxious chemicals in an attempt to stave off the invaders.

Jingsong Xu and colleagues identify an intracellular signaling molecule, called MYLK, that is required for neutrophil movement. MYLK links the ‘danger’ signals sensed outside cells to their intracellular structure, allowing them to change shape and direction, as well as increasing their ‘adhesive’ properties needed to crawl through blood vessels.

Xu’s group shows MYLK-deficient neutrophils are less able to enter lung tissues in response to septic infections. However, this defect is not a bad thing as neutrophil-mediated collateral damage is the leading cause of acute respiratory distress syndrome (ARDS), a potential lethal complication of sepsis-induced lung injury. By identifying the signaling pathway between MYLK and the cell structure, scientists can start to develop potential new targets for treating ARDS.

doi: 10.1038/ni.1628 | Original article

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