Abstract
Abstract DC development requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little is known regarding other cytokines that may control this process. In our study, we have addressed the effect of IL-2 on DC development. We have shown that the addition of IL-2 to flt3L-stimulated bone marrow (BM) cultures can block the development of both pDCs (CD11c+SiglecH+) and cDCs (CD11c+CD11b+), while expanding the populations of NK/NKT/T cells (CD3+/-NK1.l+/-). By sorting for DC precursors that are Lineage- flt3+ CD11c-, we confirm that IL-2 blocks DC development by acting directly on DC precursors, and not indirectly via its effect on NK/NKT/T cells. The inhibition of DC development by IL-2 is dependent on both the IL-2R alpha and beta chains, and STAT5. IL-2 treatment of DC precursors leads to a decrease in the expression of various transcription factors crucial for DC development. In addition, our ongoing studies indicate that the presence of IL-2 during flt3L-dependent DC development also alters the phenotype of DCs. Together our data has indicated that IL-2 inhibits the development of DCs, and suggests IL-2 can also alter DC phenotype. This has important implications in the therapeutic use of IL-2, as well as our current understanding on factors that can lead to the loss of immune tolerance in various autoimmune diseases.
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