Flt3-ITD alters the cell surface phenotype of splenic cDCs.
To characterize how constitutive Flt3 signaling impacts cDC function,
cell surface levels of classical DC markers were investigated. Integrins
or adhesion molecules (CD11c, CD11b, CD103, CD24), phenotypic molecules
(CD8), inhibitory receptors (signal-regulatory protein α, SIRPα), MHC
molecules (MHC I and II), costimulatory molecules (CD86, CD80, CD40 and
CD24), co-inhibitory molecules (PD-L1), chemokine receptors (XCR1) and
endocytic receptors (DEC205, Clec9A, Clec12A) were analyzed
(Figure 3, Supplementary Figure 3 ). Significantly increased
surface expression of MHC I, MHC II, CD103 was observed on most
Flt3ITD/ITD cDC subsets. This was accompanied by lower
CD11c, CD8, Clec9A, DEC205 and PD-L1 and varied expression of Clec12A.
While Flt3+/+ cDC2 do not express Clec12A, it was
detected at the surface of Flt3ITD/ITD cDC2.
Confirming genetic profiling of Flt3+/+ NC cDC1s (26),
these cells had reduced surface CD103, DEC205 and CD86, in addition to
reduced Clec9A, MHC II and CD40 in comparison to other
Flt3+/+ cDC subsets.