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The autophagy level of cancer cells is negatively correlated with the extent of DC activation in patients with PDAC. A, Analysis of a publicly available scRNA-seq dataset generated by Peng and colleagues (CRA001160; ref. 45), which contains data from 24 primary human PDAC tumors and 10 control pancreases. B, The myeloid cluster (C4) was reclustered into nine clusters. Clusters of “0,” “5,” and “8” were identified as DCs. C, The expression levels of gene sets related to DC functions were analyzed in the overall DC cluster. The expression levels of representative genes are shown as violin plots. The “antigen-presenting score” and “IFN-induced score” were calculated for the comparison of the “autophagy-high” and “autophagy-low” groups. D, The T-cell cluster (C3) was reclustered into seven clusters. E, T cells were divided into cells derived from the autophagy-high group (red) and those derived from the autophagy-low group (green). F, The ratio of <t>CD8</t> + T cells to Tregs (%) in the autophagy-high and autophagy-low groups. G, IF analysis of 39 PDAC patient samples. Autophagy levels in cancer cells were evaluated by staining for LC3AB (red) and CK19 (green). Representative images are shown. H, Kaplan–Meier overall survival analysis of patients with PDAC according to their cancer cell autophagy levels, defined by the ratio of LC3AB + CK19 + cells to CK19 + cells. I and J, Representative IF images of activated DCs, expressing CD11c (red) and MHC I/II (green). K, Kaplan–Meier overall survival analysis of activated DCs, defined by the ratio of MHC I + CD11c + cells to DAPI + cells from I and MHC II + CD11c + cells to DAPI + cells from J . L, Spearman correlation between the autophagy levels of cancer cells (% LC3AB + CK19 + cells/CK19 + cells) and activated DCs (% MHC I + CD11c + cells/DAPI + cells or % MHC II + CD11c + cells/DAPI + cells). Scale bars, 100 μm ( G , I , and J ). Bars, median; boxplots show a centerline, median; box limits, upper and lower quartiles; whiskers that extend up to 1.5× the IQR beyond the upper and lower quartiles ( C ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; analyzed using the Wilcoxon rank-sum test ( C ), Student t test ( F ), and log-rank test ( H and K ).
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The autophagy level of cancer cells is negatively correlated with the extent of DC activation in patients with PDAC. A, Analysis of a publicly available scRNA-seq dataset generated by Peng and colleagues (CRA001160; ref. 45), which contains data from 24 primary human PDAC tumors and 10 control pancreases. B, The myeloid cluster (C4) was reclustered into nine clusters. Clusters of “0,” “5,” and “8” were identified as DCs. C, The expression levels of gene sets related to DC functions were analyzed in the overall DC cluster. The expression levels of representative genes are shown as violin plots. The “antigen-presenting score” and “IFN-induced score” were calculated for the comparison of the “autophagy-high” and “autophagy-low” groups. D, The T-cell cluster (C3) was reclustered into seven clusters. E, T cells were divided into cells derived from the autophagy-high group (red) and those derived from the autophagy-low group (green). F, The ratio of CD8 + T cells to Tregs (%) in the autophagy-high and autophagy-low groups. G, IF analysis of 39 PDAC patient samples. Autophagy levels in cancer cells were evaluated by staining for LC3AB (red) and CK19 (green). Representative images are shown. H, Kaplan–Meier overall survival analysis of patients with PDAC according to their cancer cell autophagy levels, defined by the ratio of LC3AB + CK19 + cells to CK19 + cells. I and J, Representative IF images of activated DCs, expressing CD11c (red) and MHC I/II (green). K, Kaplan–Meier overall survival analysis of activated DCs, defined by the ratio of MHC I + CD11c + cells to DAPI + cells from I and MHC II + CD11c + cells to DAPI + cells from J . L, Spearman correlation between the autophagy levels of cancer cells (% LC3AB + CK19 + cells/CK19 + cells) and activated DCs (% MHC I + CD11c + cells/DAPI + cells or % MHC II + CD11c + cells/DAPI + cells). Scale bars, 100 μm ( G , I , and J ). Bars, median; boxplots show a centerline, median; box limits, upper and lower quartiles; whiskers that extend up to 1.5× the IQR beyond the upper and lower quartiles ( C ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; analyzed using the Wilcoxon rank-sum test ( C ), Student t test ( F ), and log-rank test ( H and K ).

Journal: Cancer Research

Article Title: Combined Autophagy Inhibition and Dendritic Cell Recruitment Induces Antitumor Immunity and Enhances Immune Checkpoint Blockade Sensitivity in Pancreatic Cancer

doi: 10.1158/0008-5472.CAN-24-0830

Figure Lengend Snippet: The autophagy level of cancer cells is negatively correlated with the extent of DC activation in patients with PDAC. A, Analysis of a publicly available scRNA-seq dataset generated by Peng and colleagues (CRA001160; ref. 45), which contains data from 24 primary human PDAC tumors and 10 control pancreases. B, The myeloid cluster (C4) was reclustered into nine clusters. Clusters of “0,” “5,” and “8” were identified as DCs. C, The expression levels of gene sets related to DC functions were analyzed in the overall DC cluster. The expression levels of representative genes are shown as violin plots. The “antigen-presenting score” and “IFN-induced score” were calculated for the comparison of the “autophagy-high” and “autophagy-low” groups. D, The T-cell cluster (C3) was reclustered into seven clusters. E, T cells were divided into cells derived from the autophagy-high group (red) and those derived from the autophagy-low group (green). F, The ratio of CD8 + T cells to Tregs (%) in the autophagy-high and autophagy-low groups. G, IF analysis of 39 PDAC patient samples. Autophagy levels in cancer cells were evaluated by staining for LC3AB (red) and CK19 (green). Representative images are shown. H, Kaplan–Meier overall survival analysis of patients with PDAC according to their cancer cell autophagy levels, defined by the ratio of LC3AB + CK19 + cells to CK19 + cells. I and J, Representative IF images of activated DCs, expressing CD11c (red) and MHC I/II (green). K, Kaplan–Meier overall survival analysis of activated DCs, defined by the ratio of MHC I + CD11c + cells to DAPI + cells from I and MHC II + CD11c + cells to DAPI + cells from J . L, Spearman correlation between the autophagy levels of cancer cells (% LC3AB + CK19 + cells/CK19 + cells) and activated DCs (% MHC I + CD11c + cells/DAPI + cells or % MHC II + CD11c + cells/DAPI + cells). Scale bars, 100 μm ( G , I , and J ). Bars, median; boxplots show a centerline, median; box limits, upper and lower quartiles; whiskers that extend up to 1.5× the IQR beyond the upper and lower quartiles ( C ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; analyzed using the Wilcoxon rank-sum test ( C ), Student t test ( F ), and log-rank test ( H and K ).

Article Snippet: After blocking, the sections of murine PDAC tissues were stained with anti-CD11c (1:500) and anti-MHC II (I-A/I-E; 1:500, #14-5321-85, Invitrogen), or anti-CD8a (1:400) and anti-granzyme B (1:500, #14-8822-82, Invitrogen), or anti-CD8a and anti-perforin (1:500, ab16074, Abcam), or anti-CD8a and anti–LAG-3 (1:500, AF3328, Novus Biologicals) antibodies, diluted in 1% BSA, overnight at 4°C.

Techniques: Activation Assay, Generated, Control, Expressing, Comparison, Derivative Assay, Staining

Combination of autophagy inhibition and DC induction synergistically suppresses tumor growth. A, Schematic outline of the in vivo vaccination experiment. B, Individual tumor growth curves and the corresponding quantification (on day 20) of the secondary challenge tumors from mice vaccinated with vehicle, KPC1 shNC, or KPC1 shATG7. C, Flow cytometry analysis of tumor-infiltrating lymphocytes in the secondary challenge tumors. D, Schematic outline of the experimental procedure used to evaluate antigen-specific CD8 + T cells in vivo . E and F, KPC1-OVA shNC or shATG7 tumors were orthotopically transplanted into C57BL/6 mice. Fourteen days later, the spleens were resected and analyzed by flow cytometry; DCs presenting the OVA-derived peptide SIINFEKL and antigen-specific CD8 + T cells bound to the H-2Kb OVA tetramer-SIINFEKL were quantified. The percentages of SIINFEKL-MHC I + DCs and antigen-specific CD8 + T cells within the total CD45 + cell population were evaluated ( E ). The percentages of SIINFEKL-MHC I + DCs/total DCs and antigen-specific CD8 + T cells/total CD8 + T cells were also assessed ( F ). G, Schematic outline of the treatment experiment used to assess the synergy between CQ and Flt3L in vivo . H–K, KPC1 tumors were orthotopically transplanted into C57BL/6 mice. Tumor-bearing mice were treated with vehicle, CQ (60 mg/kg), Flt3L (10 µg), or CQ + Flt3L. After 28 days of treatment, the tumor volumes and weights were measured ( H ). Flow cytometry was then used to determine the extent of tumor-infiltrating T-cell ( I ) and DC activation ( J ). The mean fluorescence intensities (MFI) of MHC I/II in DCs and the percentage of MHC I/II + DCs (% of DCs) are shown ( J ). IHC analysis for CD11c was performed to assess the absolute number of DCs infiltrating in tumors ( K ). Scale bars, 100 μm ( K ). Bars, median; Error bars, mean ± SD. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.001; analyzed using the one-way ANOVA ( C and H–J ), Student t test or Mann–Whitney test ( B , E , F , and K ). ( A, D, and G, Created with BioRender.com .)

Journal: Cancer Research

Article Title: Combined Autophagy Inhibition and Dendritic Cell Recruitment Induces Antitumor Immunity and Enhances Immune Checkpoint Blockade Sensitivity in Pancreatic Cancer

doi: 10.1158/0008-5472.CAN-24-0830

Figure Lengend Snippet: Combination of autophagy inhibition and DC induction synergistically suppresses tumor growth. A, Schematic outline of the in vivo vaccination experiment. B, Individual tumor growth curves and the corresponding quantification (on day 20) of the secondary challenge tumors from mice vaccinated with vehicle, KPC1 shNC, or KPC1 shATG7. C, Flow cytometry analysis of tumor-infiltrating lymphocytes in the secondary challenge tumors. D, Schematic outline of the experimental procedure used to evaluate antigen-specific CD8 + T cells in vivo . E and F, KPC1-OVA shNC or shATG7 tumors were orthotopically transplanted into C57BL/6 mice. Fourteen days later, the spleens were resected and analyzed by flow cytometry; DCs presenting the OVA-derived peptide SIINFEKL and antigen-specific CD8 + T cells bound to the H-2Kb OVA tetramer-SIINFEKL were quantified. The percentages of SIINFEKL-MHC I + DCs and antigen-specific CD8 + T cells within the total CD45 + cell population were evaluated ( E ). The percentages of SIINFEKL-MHC I + DCs/total DCs and antigen-specific CD8 + T cells/total CD8 + T cells were also assessed ( F ). G, Schematic outline of the treatment experiment used to assess the synergy between CQ and Flt3L in vivo . H–K, KPC1 tumors were orthotopically transplanted into C57BL/6 mice. Tumor-bearing mice were treated with vehicle, CQ (60 mg/kg), Flt3L (10 µg), or CQ + Flt3L. After 28 days of treatment, the tumor volumes and weights were measured ( H ). Flow cytometry was then used to determine the extent of tumor-infiltrating T-cell ( I ) and DC activation ( J ). The mean fluorescence intensities (MFI) of MHC I/II in DCs and the percentage of MHC I/II + DCs (% of DCs) are shown ( J ). IHC analysis for CD11c was performed to assess the absolute number of DCs infiltrating in tumors ( K ). Scale bars, 100 μm ( K ). Bars, median; Error bars, mean ± SD. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.001; analyzed using the one-way ANOVA ( C and H–J ), Student t test or Mann–Whitney test ( B , E , F , and K ). ( A, D, and G, Created with BioRender.com .)

Article Snippet: After blocking, the sections of murine PDAC tissues were stained with anti-CD11c (1:500) and anti-MHC II (I-A/I-E; 1:500, #14-5321-85, Invitrogen), or anti-CD8a (1:400) and anti-granzyme B (1:500, #14-8822-82, Invitrogen), or anti-CD8a and anti-perforin (1:500, ab16074, Abcam), or anti-CD8a and anti–LAG-3 (1:500, AF3328, Novus Biologicals) antibodies, diluted in 1% BSA, overnight at 4°C.

Techniques: Inhibition, In Vivo, Flow Cytometry, Derivative Assay, Activation Assay, Fluorescence, MANN-WHITNEY

Autophagy inhibition in cancer cells induces exhaustion of tumor-infiltrating CD8 + T cells, characterized by high LAG3 expression. A, scRNA-seq analysis of CD8 + T cells from the immune cell populations shown in . CD8 + T cells were reclustered into three clusters. B, Expression of key signature genes used to identify the specific CD8 + T-cell clusters. C and D, The expression levels of gene sets related to CD8 + T-cell function was analyzed in the Prolif ( C ), Prog. Exh, and Term. Exh ( D ) CD8 + T cells. “Proliferation score,” “effector signature score” ( C ), and “exhaustion signature score” ( D ) were calculated using the gene sets listed in Supplementary Table S9. E and F, Representative IF images of orthotopic syngeneic KPC1 shNC/shATG7 tumors ( E ) and orthotopic syngeneic KPC1 tumors treated with the combination therapy (CQ ± Flt3L; F ). Red, CD8a; green, LAG3. Quantification of LAG3 + CD8a + cells/DAPI + cells (%) and LAG3 + CD8a + cells/CD8a + cells (%) is shown. G, The expression levels of featured genes related to T-cell exhaustion were analyzed in exhausted CD8 + T-cell clusters (“5” and “6” in ) in human PDAC scRNA-seq data. Scale bars, 100 µm ( E and F ). Bars, median; boxplots show a centerline, median; box limits, upper and lower quartiles; whiskers that extend up to 1.5× the IQR beyond the upper and lower quartiles ( C , D , and G ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; analyzed using the Wilcoxon rank-sum test ( C , D , and G ), Student t test ( E ), and one-way ANOVA ( F ).

Journal: Cancer Research

Article Title: Combined Autophagy Inhibition and Dendritic Cell Recruitment Induces Antitumor Immunity and Enhances Immune Checkpoint Blockade Sensitivity in Pancreatic Cancer

doi: 10.1158/0008-5472.CAN-24-0830

Figure Lengend Snippet: Autophagy inhibition in cancer cells induces exhaustion of tumor-infiltrating CD8 + T cells, characterized by high LAG3 expression. A, scRNA-seq analysis of CD8 + T cells from the immune cell populations shown in . CD8 + T cells were reclustered into three clusters. B, Expression of key signature genes used to identify the specific CD8 + T-cell clusters. C and D, The expression levels of gene sets related to CD8 + T-cell function was analyzed in the Prolif ( C ), Prog. Exh, and Term. Exh ( D ) CD8 + T cells. “Proliferation score,” “effector signature score” ( C ), and “exhaustion signature score” ( D ) were calculated using the gene sets listed in Supplementary Table S9. E and F, Representative IF images of orthotopic syngeneic KPC1 shNC/shATG7 tumors ( E ) and orthotopic syngeneic KPC1 tumors treated with the combination therapy (CQ ± Flt3L; F ). Red, CD8a; green, LAG3. Quantification of LAG3 + CD8a + cells/DAPI + cells (%) and LAG3 + CD8a + cells/CD8a + cells (%) is shown. G, The expression levels of featured genes related to T-cell exhaustion were analyzed in exhausted CD8 + T-cell clusters (“5” and “6” in ) in human PDAC scRNA-seq data. Scale bars, 100 µm ( E and F ). Bars, median; boxplots show a centerline, median; box limits, upper and lower quartiles; whiskers that extend up to 1.5× the IQR beyond the upper and lower quartiles ( C , D , and G ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; analyzed using the Wilcoxon rank-sum test ( C , D , and G ), Student t test ( E ), and one-way ANOVA ( F ).

Article Snippet: After blocking, the sections of murine PDAC tissues were stained with anti-CD11c (1:500) and anti-MHC II (I-A/I-E; 1:500, #14-5321-85, Invitrogen), or anti-CD8a (1:400) and anti-granzyme B (1:500, #14-8822-82, Invitrogen), or anti-CD8a and anti-perforin (1:500, ab16074, Abcam), or anti-CD8a and anti–LAG-3 (1:500, AF3328, Novus Biologicals) antibodies, diluted in 1% BSA, overnight at 4°C.

Techniques: Inhibition, Expressing, Cell Function Assay

Triple-therapy consisting of CQ, Flt3L, and aLAG3 markedly reduces the growth of orthotopic syngeneic PDAC tumors. A, Schematic outline of the triple treatment protocol involving CQ, Flt3L, and aLAG3. B–D, KPC2 cells were orthotopically transplanted into C57BL/6 mice. Tumor-bearing mice were treated with vehicle, aLAG3 (50 µg), CQ (60 mg/kg) + Flt3L (10 µg), or CQ + Flt3L + aLAG3. After 28 days of treatment, the tumor volumes and weights were measured ( B ). IF was used to characterize cytotoxic CD8 + T cells as granzyme B + CD8a + T cells (red, CD8a; green, granzyme B; C ) and perforin + CD8a + T cells (red, CD8a; green, perforin; D ). Representative images are shown. Quantification of granzyme B + CD8a + cells/DAPI + cells (%) and granzyme B + CD8a + cells/CD8a + cells (%; C ); and perforin + CD8a + cells/DAPI + cells (%) and perforin + CD8a + cells/CD8a + cells (%; D ) is shown in the bar graphs under the corresponding IF images. Scale bars, 100 µm ( C and D ). Bars, median; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant; analyzed using one-way ANOVA ( B–D ). ( A, Created with BioRender.com .)

Journal: Cancer Research

Article Title: Combined Autophagy Inhibition and Dendritic Cell Recruitment Induces Antitumor Immunity and Enhances Immune Checkpoint Blockade Sensitivity in Pancreatic Cancer

doi: 10.1158/0008-5472.CAN-24-0830

Figure Lengend Snippet: Triple-therapy consisting of CQ, Flt3L, and aLAG3 markedly reduces the growth of orthotopic syngeneic PDAC tumors. A, Schematic outline of the triple treatment protocol involving CQ, Flt3L, and aLAG3. B–D, KPC2 cells were orthotopically transplanted into C57BL/6 mice. Tumor-bearing mice were treated with vehicle, aLAG3 (50 µg), CQ (60 mg/kg) + Flt3L (10 µg), or CQ + Flt3L + aLAG3. After 28 days of treatment, the tumor volumes and weights were measured ( B ). IF was used to characterize cytotoxic CD8 + T cells as granzyme B + CD8a + T cells (red, CD8a; green, granzyme B; C ) and perforin + CD8a + T cells (red, CD8a; green, perforin; D ). Representative images are shown. Quantification of granzyme B + CD8a + cells/DAPI + cells (%) and granzyme B + CD8a + cells/CD8a + cells (%; C ); and perforin + CD8a + cells/DAPI + cells (%) and perforin + CD8a + cells/CD8a + cells (%; D ) is shown in the bar graphs under the corresponding IF images. Scale bars, 100 µm ( C and D ). Bars, median; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant; analyzed using one-way ANOVA ( B–D ). ( A, Created with BioRender.com .)

Article Snippet: After blocking, the sections of murine PDAC tissues were stained with anti-CD11c (1:500) and anti-MHC II (I-A/I-E; 1:500, #14-5321-85, Invitrogen), or anti-CD8a (1:400) and anti-granzyme B (1:500, #14-8822-82, Invitrogen), or anti-CD8a and anti-perforin (1:500, ab16074, Abcam), or anti-CD8a and anti–LAG-3 (1:500, AF3328, Novus Biologicals) antibodies, diluted in 1% BSA, overnight at 4°C.

Techniques: