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1.
Fig. 6.

Fig. 6. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

Accumulation of CD3+ T cells in cancer cell-containing regions of PDA induced by AMD3100 and α-PD-L1. Tissue sections from PDA tumors taken from mice that had been treated for 24 h with PBS, α-PD-L1, AMD3100 high, or AMD3100 high + α-PD-L1 were stained for CD3 and p53 and analyzed by IF microscopy.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.
2.
Fig. 4.

Fig. 4. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

FAP+ cell-derived CXCL12 and T-cell exclusion. (A) Tissue sections from PDA tumors were stained for CD3, p53, and CD11b and then analyzed by IF microscopy. White arrows demonstrate examples of CD3+ cells. (B) Tissue sections from PDA tumors were stained for CXCL12 and p53 and analyzed by IF microscopy. (C) Single-cell suspensions of PDA tumors (n = 3) were stained with antibodies for FAP, CD45, and CD11b. FAP+ cells, CD11b+ cells, and PDA/PanIN cells (FAPCD45CD11b) were FACS-purified. Their levels of Cxcl12 mRNA were assessed by qRT-PCR. *P < 0.05.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.
3.
Fig. 2.

Fig. 2. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

Characterization of FAP+ stromal cells in murine PDA. (A) Tissue sections from PDA tumors were stained for FAP, CK19, and p53 and then analyzed by immunofluorescent (IF) microscopy. White arrows indicate examples of p53+ LOH cells. (B) Tissue sections from PDA tumors were stained for αSMA and FAP and analyzed by IF microscopy. (C) Single-cell suspensions of PDA tumor cells were analyzed by flow cytometry. (D) Heat map presents the reads per kilobase of transcript per million mapped reads of RNA-seq analyses of FACS-purified FAP+ cells.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.
4.
Fig. 1.

Fig. 1. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

Immunological characteristics of murine PDA. (A) Increase in PDA volume (mean ± SEM) following treatment of mice with α-PD-L1 (n = 6), α-CTLA-4 (n = 6), or control (n = 4) antibodies was measured by ultrasound. (BD) Induction of IFN-γ secretion by splenic CD8+ T cells from various donor types following stimulation by different sources of pancreatic cells was measured by ELISpot assay (n ≥ 8 in B and D; Mann–Whitney test, n = 4 in C). *P < 0.05; ***P < 0.001.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.
5.
Fig. 3.

Fig. 3. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

Conditional depletion of FAP+ stromal cells and immune control of PDA. (A) KPCD mice with PDA received DTx or PBS; after 6 d, tumoral Fap mRNA was measured by quantitative RT-PCR (qRT-PCR) (PBS, n = 5; DTx, n = 7). (B) KPC mice with or without the DTR BAC transgene received DTx or PBS, and tumor volumes were measured by ultrasound (PBS, n = 6; DTx, n = 8; DTx to non-DTR transgenic, n = 4). (C) KPCD mice with PDA received CD4- and CD8-depleting antibodies or control IgG before and during treatment with DTx or PBS. Tumor volumes were measured (α-CD4/8 + PBS, n = 3; α-CD4/8 + DTx, n = 5; isotype IgG + DTx, n = 5). (D) KPCD mice with PDA received α-CTLA-4 or α-PD-L1 during treatment with DTx or PBS, and tumor volumes were measured [DTx, n = 13 (representing all DTx-treated KPCD mice presented in B and C); α-CTLA-4 + DTx, n = 6; α-PD-L1 + DTx, n = 4]. (E) Waterfall plots demonstrate the final tumor volume changes in individual mice. Dashed lines indicate the mean tumor volume for each treatment group. *P < 0.05; **P < 0.01.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.
6.
Fig. 5.

Fig. 5. From: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.

Inhibition of CXCR4 by AMD3100 and immune elimination of PDA cells. (A) PDA-bearing mice, some of which had been pretreated with depleting CD4 and CD8 antibodies or control IgG, received PBS or AMD3100 by continuous infusion, and tumor volumes were measured by ultrasound (PBS, n = 5; AMD3100 + isotype IgG, n = 6; AMD3100 + α-CD4/8, n = 4). (B) PBS or AMD3100 (high dose) was given to PDA-bearing mice that were treated with α-CTLA-4, α-PD-L1, or control IgG (AMD3100 high + α-CTLA-4, n = 4; AMD3100 high + α-PD-L1, n = 7; AMD3100 high + isotype IgG, n = 6). (C) Waterfall plots present the final changes in tumor volumes in individual mice from A and B. Dashed lines indicate the mean tumor volume for each treatment group. (D) Tissue sections from PDA tumors taken from mice treated with PBS or AMD3100 high + α-PD-L1 for 6 d were stained for p53, and the entire cross-sections were imaged. White squares show the regions corresponding to the magnified images. Tissue sections from PDA tumors of mice treated with AMD3100 high + α-PD-L1 or PBS for 6 d were stained for Ki67 (E) or CD45 and CK19 (F) and analyzed by IF microscopy. *P < 0.05; **P < 0.01.

Christine Feig, et al. Proc Natl Acad Sci U S A. 2013 December 10;110(50):20212-20217.

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