ATP Release Guides Neutrophil Chemotaxis via P2Y2 and A3 Receptors

By Yu Chen, Ross Corriden, Y. Inoue, Linda Yip, N. Hashiguchi, A. Zinkernagel, V. Nizet, P. Insel, W. Junger. Science, 2006

892 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/55d51f5e8a280286aeffd12c3ff522c7346f69b1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. H. Hammad
2. J. Zindel
3. M. Willart
4. P. Kubes
5. B. Lambrecht

In Neurology

1. J. Zindel
2. W. Junger
3. P. Kubes

In Physiology

1. P. Pacher
2. Luca Antonioli
3. H. Hammad
4. E. Vizi
5. G. Haskó
6. B. Fredholm
7. W. Junger
8. P. Kubes

Citations in the corpus

• Extracellular ATP triggers and maintains asthmatic airway inflammation by activating dendritic cells (2007, background): “Notably, the levels of the major eosinophil (CCL11, CCL24)- and Th2 lymphocyte (CCL17, CCL22)-selective chemokines were not reduced upon apyrase treatment, suggesting that ATP is more likely to control the responsiveness of inflammatory cells to chemokine gradients, as recently suggested by in vitr”
• Immune cell regulation by autocrine purinergic signalling (2011, background): “Neutrophils release ATP in response to chemotactic mediators, and autocrine signalling through purinergic receptors regulates the chemotaxis of these cell”
• DAMPs, PAMPs, and LAMPs in Immunity and Sterile Inflammation. (2020, background): “This autocrine signal has been reported to occur via neutrophil-derived ATP (aDAMP) and LTB4 (a lipid mediator) acting on, respectively, neutrophil P2Y2 and LTB4 receptors (63, 67).”
• Adenosine, an endogenous distress signal, modulates tissue damage and repair (2007, background): “Recently it was shown that migration of neutrophils depends on release of ATP, which activates an ATP receptor as well as adenosine A3 receptors on the leading edge of the migration neutrophil leukocyte.(56) Indeed, the adenosine A3 receptors were found to traffic from intracellular sites to the lea”
• CD39 and CD73 in immunity and inflammation (2013, positive): “Several lines of evidence support the view that these events are subjected to control and coordination by ATP and adenosine that, once released from neutrophils, act in an autocrine fashion to regulate neutrophil functions, often with opposite outcomes [53].”