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. 2019 Apr 18;216(6):1359–1376. doi: 10.1084/jem.20180660

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© 2019 Medina et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 4. — Kit oncogene inhibition leads to the accumulation of CD103⁺CD11b⁻ DC progenitors. (A–E) Kit^V558Δ/+ mice were treated with vehicle or imatinib for 1 wk and analyzed for (A) frequency of Lin⁻CSF1R⁺CD117⁺MHC II⁻CD11c⁻CD135⁺ MDPs and lin⁻CSF1R⁺CD117^intMHC II⁻CD11c⁻CD135⁺ CDPs in the bone marrow (five mice/group); (B) Lin⁻CD11c⁺MHC II⁻CD135⁺SIRPα^int preDCs in the bone marrow (four mice/group); (C) Lin⁻CD11c⁺MHC II⁻CD135⁺SIRPα^int preDCs in the peripheral blood (four mice/group); (D) Siglec F⁻F4/80⁻CD11c⁺MHC II⁺CD103⁺CD11b⁻ DCs in the liver (five mice/group); and (E) CD11c⁺MHC II⁺CD8α⁺ DCs in the spleen (five mice/group). A–E are representative of two independent experiments. (F) Flow cytometry and frequency of DC subsets in tumors were analyzed in Kit^{V558Δ;T669I/+} mice treated with vehicle or imatinib for 1 wk (six mice/group pooled from two independent experiments). (G) S2 cells were injected into the flanks of wild-type mice. After 3 wk of growth, imatinib was administered for 1 wk. Flow cytometry and frequency of DC subsets were analyzed (five mice/group, representative of two independent experiments). (H) Tumors of Kit^V558Δ/+ mice treated with vehicle or imatinib for 1 or 4 wk were analyzed by flow cytometry for DC populations. Red box identifies CD103⁻CD11b⁻ DCs. Graph represents frequency of CD103⁻CD11b⁻ DCs as a percentage of CD45⁺ cells (four to five mice/group, representative of two independent experiments). (I) Flow cytometry of CD103⁻CD11b⁻ DCs distinguished by CD24 and SIRPα expression in tumors of untreated Kit^V558⁻^/+ mice. Histograms represent transcription factor expression within these subsets. Histogram color matches gating within the CD103⁻CD11b⁻ DC compartment (five mice/group). (J) CD86, CD80, and CD40 MFI in CD24^hiSIRPα⁻ progenitors and CD103⁺CD11b⁻ DCs in tumors of untreated Kit^V558Δ/+ mice (five mice/group). I and J are representative of two independent experiments. (K) Untreated tumors in Kit^V558Δ/+;Batf3^+/+ and Kit^V558Δ/+;Batf3⁻^/⁻ mice were analyzed for frequency of CD24^hiSIRPα⁻ progenitors (three mice/group, representative of two independent experiments). (L) Frequency of CD24^hiSIRPα⁻ progenitors and IRF8⁺ progenitors in tumors of Kit^V558Δ/+ mice treated with vehicle or imatinib for 1 wk (four mice/group, representative of two independent experiments). (M) Frequency of CD24^hiSIRPα⁻ progenitors as a percentage of CD45⁺ or CD103⁻CD11b⁻ DCs in tumors of Kit^V558Δ/+ mice treated with vehicle or imatinib for 1 or 4 wk (four to five mice/group, similar results obtained in experiments separately analyzing 1- and 4-wk treatment durations). Data represent mean ± SEM; P values were calculated using a Student’s t test; *, P < 0.05. n.s., not significant.