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Article . 2018 . Peer-reviewed
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DNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitment

Authors: del Fresno, Carlos; Saz-Leal, Paula; Enamorado, Michel; Wculek, Stefanie K.; Martínez-Cano, Sarai; Blanco-Menéndez, Noelia; Schulz, Oliver; +5 Authors

DNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitment

Abstract

The absence of DNGR-1 is dangerous Conventional type 1 dendritic cells (cDC1s) can sense tissue damage via DNGR-1, which binds F-actin exposed by necrotic cells. DNGR-1 activation favors cross-presentation, the process by which extracellular antigens are processed and presented to CD8 + T cells via major histocompatibility complex class I molecules. Del Fresno et al. studied mice lacking DNGR-1 and found that DNGR-1 also has anti-inflammatory effects (see the Perspective by Salazar and Brown). It inhibits the secretion of the chemokine CXCL2 by cDC1s, which, in turn, limits neutrophil recruitment. Thus, DNGR-1 connects cell-death sensing with a mechanism of damage control. Science , this issue p. 351 ; see also p. 292

Keywords

Pancreatitis, Acute Necrotizing, Candidiasis, Dendritic Cells, Mice, Mutant Strains, Mice, Necrosis, Neutrophil Infiltration, Candida albicans, Animals, Lectins, C-Type, Receptors, Immunologic, Pancreas

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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