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The receptor Flt3 and its ligand Flt3L are both critical for dendritic cell (DC) development, but DC deficiency is more severe in Flt3l -/-  mice than in Flt3 -/-  mice. This has led to speculation that Flt3L binds to another receptor that also supports DC development. However, we found that Flt3L administration does not generate DCs in Flt3 -/-  mice, arguing against a second receptor. Instead, Flt3 -/-  DC progenitors matured in response to macrophage colony-stimulating factor (M-CSF) or stem cell factor, and deletion of Csf1r in Flt3 -/-  mice further reduced DC development, indicating that these cytokines could compensate for Flt3. Surprisingly, Flt3 -/-  DC progenitors displayed enhanced M-CSF signaling, suggesting that loss of Flt3 increased responsiveness to other cytokines. In agreement, deletion of Flt3 in Flt3l -/-  mice paradoxically rescued their severe DC deficiency. Thus, multiple cytokines can support DC development, and the discrepancy between Flt3 -/-  and Flt3l -/-  mice results from the increased sensitivity of Flt3 -/-  progenitors to these cytokines.

Altered compensatory cytokine signaling underlies the discrepancy between Flt3–/– and Flt3l–/– mice