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Del Fresno, Carlos; 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; Sancho, David
Science (American Association for the Advancement of Science), 10/2018, Letnik: 362, Številka: 6412Journal Article
Host 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 , 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 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 ) production by cDC1s during 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.
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in: SICRIS
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