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

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