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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2015 ; 10
(3
): e0121968
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gab.com Text
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English Wikipedia
Migration of myeloid cells during inflammation is differentially regulated by the
cell surface receptors Slamf1 and Slamf8
#MMPMID25799045
Wang G
; van Driel BJ
; Liao G
; O'Keeffe MS
; Halibozek PJ
; Flipse J
; Yigit B
; Azcutia V
; Luscinskas FW
; Wang N
; Terhorst C
PLoS One
2015[]; 10
(3
): e0121968
PMID25799045
show ga
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.