Skip to main content
. Author manuscript; available in PMC: 2016 Dec 16.
Published in final edited form as: Curr Opin Immunol. 2014 May 27;29:69–78. doi: 10.1016/j.coi.2014.04.006

Figure 1. Dendritic cells orchestrate pathogen-appropriate innate and adaptive immune responses.

Figure 1

(a and b) A pre-cDC progenitor develops into both the Batf3-dependent CD8α+ cDC and the Notch2-dependent CD11b+ cDC subsets. (a) CD8α+ cDCs respond to Toxoplasma gondii infection by sensing the antigen profilin via TLRs 11/12. Activated CD8α+ cDCs secrete IL-12 which induces IFN-γ secretion by ILC1/NK cells. IFN-γ activates infected cells, such as MΦ’s, to produce nitric oxide and reactive oxygen species, which are necessary for parasite control. In parallel, activated CD8α+ cDCs migrate to lymph nodes and promote differentiation of TH1 cells, which enhance parasite clearance. (b) Infection with Citrobacter rodentium activates CD11b+ cDCs in the small intestine by an unknown mechanism. Upon activation, tissue resident CD11b+ cDCs produce high levels of IL-23 which induces IL-22 production in Rorγt dependent ILC3s and possibly acts on other cells as well. IL-22 activates the epithelial layer to secrete the bactericidal lectin RegIIIγ, which is necessary for C. rodentium clearance. CD11b+ cDCs also migrate to the mesenteric lymph node where they induce T cell differentiation into TH17 and TH22 cells. These effector T cells migrate back to the site of infection and are the adaptive source of IL-22. cDC: classical dendritic cell. TLR: Toll-like Receptor. ILC3: Innate lymphoid cell type 3. IFN-γ: Interferon-γ. MΦ: Macrophage