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

AuthorsFresno, Carlos del; Saz-Leal, Paula; Enamorado, Michel; Wculek, Stefanie K.; Martínez-Cano, Sarai; Blanco-Menéndez, Noelia; Schulz, Oliver; Gallizioli, Mattia; Miró-Mur, Francesc; Cano, Eva; Planas, Anna M. ; Sancho, David
Issue Date19-Oct-2018
PublisherAmerican Association for the Advancement of Science
CitationScience 362(6412): 351-356 (2018)
AbstractHost injury triggers feedback mechanisms that limit tissue damage. Conventional type 1 dendritic cells (cDC1s) express dendritic cell natural killer lectin group receptor-1 (DNGR-1), encoded by the gene Clec9a, which senses tissue damage and favors cross-presentation of dead-cell material to CD8+ T cells. Here we find that DNGR-1 additionally reduces host-damaging inflammatory responses induced by sterile and infectious tissue injury in mice. DNGR-1 deficiency leads to exacerbated caerulein-induced necrotizing pancreatitis and increased pathology during systemic Candida albicans infection without affecting fungal burden. This effect is B and T cell–independent and attributable to increased neutrophilia in DNGR-1–deficient settings. Mechanistically, DNGR-1 engagement activates SHP-1 and inhibits MIP-2 (encoded by Cxcl2) production by cDC1s during Candida infection. This consequently restrains neutrophil recruitment and promotes disease tolerance. Thus, DNGR-1–mediated sensing of injury by cDC1s serves as a rheostat for the control of tissue damage, innate immunity, and immunopathology.
Publisher version (URL)https://doi.org/10.1126/science.aan8423
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