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Innate immunity

p38δ–PKD1–PTEN signalling promotes neutrophil chemotaxis

Nature Reviews Immunology volume 12, page 807 (2012)Cite this article

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A new study shows that expression of the p38 δ-isoform (a member of the mitogen-activated protein kinase family) in neutrophils is essential for neutrophil chemotaxis. p38δ-deficient neutrophils had an impaired migratory capacity in vitro and failed to infiltrate the lungs in a mouse model of acute lung injury. The effect of p38δ on neutrophil extravasation and chemotaxis involved the inactivation of protein kinase D1 (PKD1). PKD1 was shown to phosphorylate the phosphoinositide 3-kinase (PI3K) regulatory subunit p85δ, which in turn enhanced the activity of the lipid phosphatase PTEN. Thus, inactivation of PKD1 and PTEN downstream of p38δ appear to maintain the gradient of phosphatidylinositides (lipid targets of PI3K and PTEN) that is required for neutrophil chemotaxis.

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ORIGINAL RESEARCH PAPER

  1. Ittner, A. et al. Regulation of PTEN activity by p38δ-PKD1 signaling in neutrophils confers inflammatory responses in the lung. J. Exp. Med. 5 Nov 2012 (doi:10.1084/jem.20120677)

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  1. Maria Papatriantafyllou
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Papatriantafyllou, M. p38δ–PKD1–PTEN signalling promotes neutrophil chemotaxis. Nat Rev Immunol 12, 807 (2012). https://doi.org/10.1038/nri3352

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