Left panel: Proportions of DCs, CD4+FoxP3+Treg cells, and CD4+FoxP3− T cells in spleens of Flt3L-deficient (Flt3L−/−), wild-type, and Flt3L-injected mice (10 μg/day i.p. or s.c. over 10 days). Right panel: Factors involved in Flt3L-mediated DC and subsequent CD4+FoxP3+Treg cell expansion. Flt3L expands DCs from DC progenitors but does not act directly on CD4+FoxP3+Treg cells. Treg expansion is dependent on exogenous IL-2 not produced by DCs, and on direct cell contact or close proximity to DCs. The factors provided by DCs to Tregs need to be defined, but Treg expansion in experimental settings used by Swee et al is not dependent on TCR-MHCII complex interaction. Professional illustration by Kenneth X. Probst.

Left panel: Proportions of DCs, CD4+FoxP3+Treg cells, and CD4+FoxP3 T cells in spleens of Flt3L-deficient (Flt3L−/−), wild-type, and Flt3L-injected mice (10 μg/day i.p. or s.c. over 10 days). Right panel: Factors involved in Flt3L-mediated DC and subsequent CD4+FoxP3+Treg cell expansion. Flt3L expands DCs from DC progenitors but does not act directly on CD4+FoxP3+Treg cells. Treg expansion is dependent on exogenous IL-2 not produced by DCs, and on direct cell contact or close proximity to DCs. The factors provided by DCs to Tregs need to be defined, but Treg expansion in experimental settings used by Swee et al is not dependent on TCR-MHCII complex interaction. Professional illustration by Kenneth X. Probst.

Close Modal

or Create an Account

Close Modal
Close Modal