Project description:Defense against attaching and effacing (A/E) bacteria requires the sequential generation of IL-23 and IL-22 to induce protective mucosal responses. While the critical source of IL-22 has been identified as CD4+ and Nkp46+ innate lymphoid cells (ILCs), the precise source of IL-23 is unclear. Here, we use genetic techniques to deplete specific classical dendritic cell (cDC) subsets and analyze immunity to the A/E pathogen Citrobacter rodentium. We find that Zbtb46+ cDCs, and specifically Notch2-dependent intestinal CD11b+ cDCs, but not Batf3-dependent CD103+ cDCs, are required for IL-23 production and immunity against C. rodentium. Notch2 controls cDC differentiation at a terminal step mediated by lymphotoxin signaling. Importantly, these results provide the first demonstration of a non-redundant function of CD11b+ cDCs in vivo. Analysis of differentially expressed genes in ESAM+ and ESAM- CD11b+ and DEC205+ splenic classical DC subsets. Splenocytes were harvested from WT C57Bl/6 or WT Cx3cr1-gfp mice and cDC subsets sorted to >95% purity on the FACSAriaII.
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
Project description:To determine if the residual cDC subsets in the Δ1+2+3 and Δ32 mice reflected their normal counterparts, we performed bulk RNA-sequencing analysis of cDC1 and cDC2 from WT, Δ1+2+3 and Δ32 mice. cDC1 from WT and Δ1+2+3 clustered together in principal component analysis (PCA) plot, whereas cDC2 from WT and Δ32 mice cluster together. Further, cDC1 and cDC2 from WT mice show a large number of differentially expressed genes (DEGs), as expected. However, there were few DEGs in cDC1 between WT and Δ1+2+3 mice, or in cDC2 between WT and Δ32 mice, indicating no substantive transcriptional differences between corresponding cDC subsets in WT, Δ32 and Δ1+2+3 mice.
