Migration of Myeloid Cells during Inflammation Is Differentially Regulated by the Cell Surface Receptors Slamf1 and Slamf8

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Migration of Myeloid Cells during Inflammation Is Differentially Regulated by the Cell Surface Receptors Slamf1 and Slamf8

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Title: Migration of Myeloid Cells during Inflammation Is Differentially Regulated by the Cell Surface Receptors Slamf1 and Slamf8
Author: Wang, Guoxing; van Driel, Boaz J.; Liao, Gongxian; O’Keeffe, Michael S.; Halibozek, Peter J.; Flipse, Jacky; Yigit, Burcu; Azcutia, Veronica; Luscinskas, Francis W.; Wang, Ninghai; Terhorst, Cox

Note: Order does not necessarily reflect citation order of authors.

Citation: Wang, G., B. J. van Driel, G. Liao, M. S. O’Keeffe, P. J. Halibozek, J. Flipse, B. Yigit, et al. 2015. “Migration of Myeloid Cells during Inflammation Is Differentially Regulated by the Cell Surface Receptors Slamf1 and Slamf8.” PLoS ONE 10 (3): e0121968. doi:10.1371/journal.pone.0121968. http://dx.doi.org/10.1371/journal.pone.0121968.
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Abstract: Previous studies have demonstrated that the cell surface receptor Slamf1 (CD150) is requisite for optimal NADPH-oxidase (Nox2) dependent reactive oxygen species (ROS) production by phagocytes in response to Gram- bacteria. By contrast, Slamf8 (CD353) is a negative regulator of ROS in response to Gram+ and Gram- bacteria. Employing in vivo migration after skin sensitization, induction of peritonitis, and repopulation of the small intestine demonstrates that in vivo migration of Slamf1-/- dendritic cells and macrophages is reduced, as compared to wt mice. By contrast, in vivo migration of Slamf8-/- dendritic cells, macrophages and neutrophils is accelerated. These opposing effects of Slamf1 and Slamf8 are cell-intrinsic as judged by in vitro migration in transwell chambers in response to CCL19, CCL21 or CSF-1. Importantly, inhibiting ROS production of Slamf8-/- macrophages by diphenyleneiodonium chloride blocks this in vitro migration. We conclude that Slamf1 and Slamf8 govern ROS–dependent innate immune responses of myeloid cells, thus modulating migration of these cells during inflammation in an opposing manner.
Published Version: doi:10.1371/journal.pone.0121968
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370648/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:15034950
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