Recently our paper titled “Integrin-Induced PIP5K1C Kinase Polarization Regulates Neutrophil Polarization, Directionality, and In Vivo Infiltration” was published on the well-known journal Immunity. It discussed the results made by our Professor Wang Ping and Professor Dan Wu of Yale University.
The paper pointed out that Neutrophils are important in innate immunity and acute inflammatory responses. However, the regulation of their recruitment to sites of inflammation has not been well characterized. They investigated the kinase PIP5K1C and showed that PIP5K1C deficiency impaired neutrophil recruitment because of an adhesion defect. PIP5K1C regulated the adhesion through facilitating RhoA GTPase and integrin activation by chemoattractants. Integrins could induce polarization of an isoform of PIP5K1C, PIP5K1C-90, in neutrophils through intracellular vesicle transport independently of exogenous chemoattractant. PIP5K1C-90 polarization was required for polarized RhoA activation at uropods and provided an initial directional cue for neutrophil polarization on the endothelium. The polarization was also required for circumventing the inhibition of lamellipodium formation by RhoA so that neutrophils could form leading edges required for transendothelial migration. Because integrins are not known to regulate neutrophil polarization, their study revealed a previously underappreciated role of integrin signaling in neutrophil regulation.
(Translated and Edited by Shui Tao. Email: tao.shui0430@gmail.com)
