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. Author manuscript; available in PMC: 2011 Oct 29.
Published in final edited form as: Immunity. 2010 Oct 7;33(4):597–606. doi: 10.1016/j.immuni.2010.09.012

Figure 4. DC-specific Pten deletion causes the expansion of CD8+ cDCs.

Figure 4

(A) Staining profiles of splenic DC populations in Ptenfl/fl Itgax-Cre+ animals with DC-specific Pten deletion (DC-PtenΔ) and in littermate controls (Ctrl), highlighting CD11clo Bst2+ pDCs, CD11chi MHC II+ cDCs and their subsets.

(B) The fraction and absolute number of cDC subsets in DC-PtenΔ and control spleens (n=10–11). The P values of statistically significant differences are indicated.

(C) The analysis of DCs in hematopoietic chimeras reconstituted with a mixture of the control or DC-PtenΔ BM (CD45.2+) and wild-type CD45.1+ competitor BM. Shown are representative staining profiles and the absolute numbers of donor- and competitor-derived splenic cDC subsets (mean ± S.D. of 3 recipient animals).

(D) Splenic cDC subsets in Cx3cr1-EGFP+ DC-PtenΔ and littermate control mice. Shown are staining profiles of CD11chi MHC II+ cDCs with EGFP+ and EGFP− CD8+ cDC subsets highlighted, and absolute numbers of cDC subsets (n=4–5).

(E) Immature splenic cDC populations in DC-PtenΔ and control mice. Shown are staining profiles of gated MHC II+ CD24+ or CD24− populations containing mature CD11chi cDC subsets as well as CD11clo CD8lo immature cDCs (mean ± S.D. of three animals).