Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion.

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Fig. 4. Primary human metastatic melanomas contain CCL21-expressing LECs, and expression of VEGFC positively correlates with hallmarks of tumor inflammation.

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Anti–4-1BB/PD-1 combination enriched CD8+ T cells in TILs

Fig. 5. Circulating PPi concentration does not correlate with severity of calcification phenotype in mice. Circulating PPi concentration does not correlate.

Fig. 2. VEGF-C/VEGFR-3 signaling increases responsiveness of melanoma to immunotherapy. VEGF-C/VEGFR-3 signaling increases responsiveness of melanoma to.

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Expansion of Bacteroides species during colitis does not enhance TCR-specific T cell responses. Expansion of Bacteroides species during colitis does not.

Fig. 8. In vivo suppression of MM by CMLD

Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.

Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.

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CAR8 failure in an OT1 TCR transgenic T cell after exposure to OVA

Fig. 2. GPC3 expression in normal and tumor tissues.

Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.

Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates.

Fig. 5 A competent Fc is required for the antitumor immune response.

Fig. 4. Antitumor efficacy of ERY974 against various cancer types.

Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.

Fig. 5 Combination intravenous reovirus and checkpoint inhibition in an orthotopic syngeneic brain tumor model. Combination intravenous reovirus and checkpoint.

Fig. 5. Serum VEGF-C correlates with antitumor immune responses and PFS after immunotherapy in human metastatic melanoma patients. Serum VEGF-C correlates.

Fig. 3 In situ vaccination with CpG and anti-OX40 is therapeutic in a spontaneous tumor model. In situ vaccination with CpG and anti-OX40 is therapeutic.

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Fig. 5 Local gel scaffold for T cell memory response.

Fig. 4. Improved tumor response to docetaxel in TNBC and trastuzumab in HER2-amplified PDX models with the addition of S Improved tumor response.

LV activation of DCs and subsequent CD8+ T cell priming are dependent on STING and cGAS but not on MyD88, TRIF, or MAVS. LV activation of DCs and subsequent.

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Stroke induces atheroprogression via the RAGE-signaling pathway

Fig. 6. pKL cells revert hyperglycemia in NOD mice in vivo.

Fig. 7. mRIPO therapy restricts tumor growth and produces antigen-specific antitumor immunity. mRIPO therapy restricts tumor growth and produces antigen-specific.

Fig. 2. IL-2/rapamycin–expanded T cells express homing receptors to traffic to lymphoma sites and are resistant to SN-38 toxicity. IL-2/rapamycin–expanded.

Fig. 4. Efficacy of C12G6 compared with and in combination with oseltamivir in mice. Efficacy of C12G6 compared with and in combination with oseltamivir.

Fig. 3. VEGFR-3 signaling increases infiltration of naïve T cells in a CCR7-dependent manner. VEGFR-3 signaling increases infiltration of naïve T cells.

Fig. 2. Exposure of both TCR and CAR antigens diminishes efficacy of CAR8 but not CAR4 cells. Exposure of both TCR and CAR antigens diminishes efficacy.

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Fig. 5 Extended local release of R848 increases the number of innate and adaptive antitumor immune cells and cytokines. Extended local release of R848.

Fig. 5 Treatment with an OX40 agonist antibody of 3-week-old HBVtgRag−/− mice or mice with chronic HBV disease results in an altered immune response to.

Anti-CD96 combines with anti–CTLA-4 or anti–PD-1 to suppress experimental and spontaneous lung metastases. Anti-CD96 combines with anti–CTLA-4 or anti–PD-1.

CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.

Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.

Fig. 5 A competent Fc is required for the antitumor immune response.

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Fig. 3 NK cells are enriched in ICB-sensitive tumors in mouse models and patients and are required for response. NK cells are enriched in ICB-sensitive.

Fig. 1. CAR4 and CAR8 cells demonstrate in vitro and in vivo antileukemic efficacy. CAR4 and CAR8 cells demonstrate in vitro and in vivo antileukemic efficacy.

Fig. 4 Rational therapeutic modulation of the tumor microenvironment sensitizes tumors to ICB. Rational therapeutic modulation of the tumor microenvironment.

Fig. 2 In situ vaccination of CpG in combination with anti-OX40 antibody cures established local and distant tumors. In situ vaccination of CpG in combination.

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CD8 T cells play a critical role in responses of TILs due to BRAF inhibition. CD8 T cells play a critical role in responses of TILs due to BRAF inhibition.

Fig. 2 Extended local release of agonists of innate immunity prevents tumor recurrence and eliminates distal metastases. Extended local release of agonists.

Fig. 3 Local Maraba treatment of TNBC tumors provides long-term systemic protection. Local Maraba treatment of TNBC tumors provides long-term systemic.

Fig. 2. PlGF-2123–144 conjugation reduces systemic exposure to checkpoint blockade Abs and potential treatment-related toxicity. PlGF-2123–144 conjugation.

Induction of a tumor-specific immune response following radiofrequency ablation (RFA). Induction of a tumor-specific immune response following radiofrequency.

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Tumor protection induced by therapeutic PLG vaccination in combination with blockade antibodies. Tumor protection induced by therapeutic PLG vaccination.

The PI3Kβ inhibitor enhances the antitumor activity of T cell–mediated immunotherapy in mice bearing PTEN loss tumors. The PI3Kβ inhibitor enhances the.

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Moderate-affinity vaccine antigens elicited greatest antitumor response. Moderate-affinity vaccine antigens elicited greatest antitumor response. Wild-type.

Enhanced antitumor effects with combination IL21 and anti–PD-1/anti–Tim-3 therapy. Enhanced antitumor effects with combination IL21 and anti–PD-1/anti–Tim-3.

The effect of βAR signaling on the generation of a cytotoxic CD8+ T-cell response in vivo. The effect of βAR signaling on the generation of a cytotoxic.

Fig. 7 Differences in the tumor microenvironment between transplant and transgenic BRAFV600E-driven melanoma models may underlie refractoriness of iBIP2.

Fig. 3 Superiority of BAFF-R versus CD19-CAR T cells in a Burkitt lymphoma model is not due to greater tumor antigen density. Superiority of BAFF-R versus.

IL2Cx alone or in combination with anti–CTLA-4 increases the CD8/Treg ratio in the tumor. IL2Cx alone or in combination with anti–CTLA-4 increases the.

Fig. 3. Association between peak CTL019 expansion and response.

Bezafibrate increases the number of effector CTLs by enhancing their survival capacity and proliferation. Bezafibrate increases the number of effector.

Phenotyping of T cells. Phenotyping of T cells. Circulating lymphocytes from a tumor-naïve C57BL/6 mice (left column) were compared with those from C57BL/6.

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Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion of TILs after therapy. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion of TILs after therapy. (A and B) B16-OVA/VC tumor–bearing mice treated with control IgG (Iso) or anti–VEGFR-3 (αR3)–blocking antibodies were euthanized 3 days after ATT, and tumor single-cell suspensions were analyzed by flow cytometry (n = 5). Quantification of overall naïve CD8+ (CD45+CD8+CD44−CD62L+), effector CD8+ (CD45+CD8+CD44+CD62L−), and OT-I (CD45+CD8+CD45.1+) T cells (A) in the tumor and (B) in the dLNs. (C) Tumor growth and survival curves of B16-OVA/VC tumor–bearing mice treated with anti-CCR7 (αCCR7), control IgG (Iso), or αR3 antibodies combined with ATT on day 9. CCR7 blockade was performed only before ATT (days 0, 3, and 6) (data pooled from two or more independent experiments, n ≥ 15 total). (D) Tumor growth curves of B16-OVA/VC tumor–bearing mice treated with control IgG (Iso) or αR3 antibodies received daily injections of the small molecular S1P inhibitor FTY720 starting on the same day as ATT was performed (day 9) (n ≥ 5). Statistics show differences between Iso + FTY720 and αR3 + FTY720 by one-way ANOVA. (E) Representative flow cytometry plots and (F) quantification of circulating CD4+ and CD8+ T cells (after B220 exclusion) in blood 26 days after tumor inoculation. *P < 0.05, **P < 0.01, ***P < 0.001 by two-tailed Student’s t test or one-way ANOVA and log-rank (Mantel-Cox) test for survival curves. Manuel Fankhauser et al., Sci Transl Med 2017;9:eaal4712 Published by AAAS