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oai:repisalud.isciii.es:20.500.12105/65022025-06-13T10:50:14Zcom_20.500.12105_19604com_20.500.12105_2051com_20.500.12105_15322com_20.500.12105_2052col_20.500.12105_19605col_20.500.12105_16961col_20.500.12105_19617

00925njm 22002777a 4500 dc del Fresno, Carlos author Sanz-Leal, Paula author Enamorado, Michel author Wculek, Stefanie K author Martinez-Cano, Sarai author Blanco-Menendez, Noelia author Schulz, Oliver author Gallizioli, Mattia author Miró-Mur, Francesc author Cano, Eva author Planas, Anna author Sancho, David author 2018-10-19 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 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. Science. 2018; 362(6412):351-356 10.1126/science.aan8423 1095-9203 0036-8075 Science 30337411 http://hdl.handle.net/20.500.12105/6502 DNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitment