Altered compensatory cytokine signaling underlies the discrepancy between Flt3^-/- and Flt3l^-/- mice.

ABSTRACT: 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 enha

SUBMITTER: Durai V 

PROVIDER: S-EPMC5940266 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature