Research ArticleCell Migration

Autocrine Purinergic Receptor Signaling Is Essential for Macrophage Chemotaxis

Sci. Signal.  27 Jul 2010:
Vol. 3, Issue 132, pp. ra55
DOI: 10.1126/scisignal.2000588

You are currently viewing the editor's summary.

View Full Text
As a service to the community, AAAS/Science has made this article free with registration.

Self-Help Migration

Immune cells such as neutrophils and macrophages migrate to sites of infection or inflammation by following gradients of chemoattractants. These include chemokines, which can be released by other cells at the target site; components of the complement system, such as C5a; and bacterial products, such as the formylated peptide, fMLP. While they navigate along the chemoattractant gradient toward their destination, cells are also exposed to other signals, some of which may compete with the chemoattractant that the cells were already following. Another level of complexity in the regulation of cell migration came from the discovery that migrating neutrophils release adenosine triphosphate (ATP), which then functions in an autocrine fashion through the purinergic receptor P2Y2 to enhance migration; cells deficient in P2Y2 have impaired gradient sensing. Kronlage et al. provide evidence that autocrine ATP signaling is also required for the migration of macrophages in vitro and in an in vivo model. The authors found that more than one type of ATP receptor type as well as metabolites of ATP contributed to the migratory responses of macrophages; furthermore, ATP was not released through pannexin-1 proteins, as has been suggested for neutrophils. Together, these data suggest that autocrine purinergic receptor signaling may play a general role in regulating the chemotactic responses of immune cells.

Cited By...