The way in which immune cells focus in on invading bacteria within infected tissues is reported online this week in Nature Immunology. The study describes a series of chemical signposts that direct neutrophils, the first responders in an immune response, to the site of infection.

Like other immune cells, neutrophils express surface receptors that sense chemical trafficking signals from damaged tissues or released by the bacteria. Activation of these receptors triggers formation of fatty molecules called PIP3, which lead to changes in the cell structure and directional movement. As the neutrophils enter infected tissues they can be surrounded by chemical signals, thus prompting a decision process for ‘which way to go’.

Paul Kubes and colleagues show neutrophils prioritize such directional signals via an intracellular enzyme called PTEN. Surface receptors that sense the bacterial signalling compounds activate PTEN, which takes control by removing phosphates from PIP3. By doing so, neutrophils ignore the previous chemical signals that guided them into the tissues and move instead towards their bacterial targets.

These results help explain how neutrophils can efficiently migrate to sites of infection.