Abstract
Classical dendritic cells (cDCs) in mice have been divided into 2 major subsets based on the expression of nuclear transcription factors: a CD8+Irf8+Batf3 dependent (DC1) subset, and a CD8-Irf4+ (DC2) subset. We found that the CD8+DC1 subset can be further divided into CD8+DC1a and CD8+DC1b subsets by differences in surface receptors, gene expression, and function. Whereas all 3 DC subsets can act alone to induce potent Th1 cytokine responses to class I and II MHC restricted peptides derived from ovalbumin (OVA) by OT-I and OT-II transgenic T cells, only the DC1b subset could effectively present glycolipid antigens to natural killer T (NKT) cells. Vaccination with OVA protein pulsed DC1b and DC2 cells were more effective in reducing the growth of the B16-OVA melanoma as compared to pulsed DC1a cells in wild type mice. In conclusion, the Batf3-/- dependent DC1 cells can be further divided into two subsets with different immune functional profiles in vitro and in vivo.
Highlights
The subset of CD8+dendritic cells (DCs) that is dependent on the basic leucine zipper transcription factor (Batf3) and Irf8 nuclear transcription factors for development and maturation in mouse lymphoid tissues has been extensively studied [1,2,3,4,5]
The DC1b cells represented the majority of DCs in both strains, and the mean percentage of Type II dendritic cell (DC2) cells was significantly higher in the BALB/c mice
Our findings show that Batf3 dependent CD8+Type I dendritic cell (DC1) cells, which had been previously distinguished from DC2 cells by the expression of surface markers such as CD24 and XCR1 [6, 20] and the nuclear transcription factor Irf8 [4, 5], can be further divided by their surface phenotype, gene expression profile and function into two subsets that we have designated DC1a and DC1b
Summary
The subset of CD8+dendritic cells (DCs) that is dependent on the Batf and Irf nuclear transcription factors for development and maturation in mouse lymphoid tissues has been extensively studied [1,2,3,4,5]. Inactivation of the gene encoding Batf-3 results in the selective elimination of CD8+ and CD103+ DC1 DCs [17, 18] Both subsets express high levels of XCR1, low levels of CD172, and can stimulate CD8+ T cell immunity [19,20,21]. The DC2 cells are predominantly Batf independent [20]
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