Kidney dendritic cells (DCs) regulate nephritogenic T cell responses. Most kidney DCs belong to the CD11b+subset and promote crescentic GN (cGN). The function of the CD103+subset, which represents <5% of kidney DCs, is poorly understood. We studied the role of CD103+DCs in cGN using several lines of genetically modified mice that allowed us to reduce the number of these cells. In all lines, we detected a reduction of FoxP3+intrarenal regulatory T cells (Tregs), which protect against cGN. Mice lacking the transcription factor Batf3 had a more profound reduction of CD103+DCs and Tregsthan did the other lines used, and showed the most profound aggravation of cGN. The conditional reduction of CD103+DC numbers by 50% in Langerin-DTR mice halved Tregnumbers, which did not suffice to significantly aggravate cGN. Mice lacking the cytokine Flt3L had fewer CD103+DCs and Tregsthan Langerin-DTR mice but exhibited milder cGN than did Batf3-/-mice presumably because proinflammatory CD11b+DCs were somewhat depleted as well. Conversely, Flt3L supplementation increased the number of CD103+DCs and Tregs, but also of proinflammatory CD11b+DCs. On antibody-mediated removal of CD11b+DCs, Flt3L supplementation ameliorated cGN. Mechanistically, CD103+DCs caused cocultured T cells to differentiate into Tregsand produced the chemokine CCL20, which is known to attract Tregsinto the kidney. Our findings show that CD103+DCs foster intrarenal FoxP3+Tregaccumulation, thereby antagonizing proinflammatory CD11b+DCs. Thus, increasing CD103+DC numbers or functionality might be advantageous in cGN.