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.

Slides:

Advertisements

Similar presentations

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

Advertisements

Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.

Fig. 5. Blocking LTB4 during initial lymphangiogenesis period abrogates the therapeutic benefit of LTB4 antagonism. Blocking LTB4 during initial lymphangiogenesis.

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

Sunitinib plus rMVA–CEA–TRICOM vaccine decreased tumor burden and increased intratumoral infiltration of T lymphocytes in the MC38-CEA colon carcinoma.

Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.

Fig. 5 Maraba induces antitumor T cell immunity.

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

Fig. 4. aPD-1 mAb transfer to macrophages is mediated by FcγRs.

Analysis of brain and spinal cord of treated Gaa−/− mice and controls

Volume 1, Issue 3, Pages (March 2012)

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

Fig. 3. A circadian rhythm in fibroblast wound-healing response.

Fig. 1 pDCs infiltrate the skin of SSc patients and spontaneously secrete IFN-α and CXCL4. pDCs infiltrate the skin of SSc patients and spontaneously secrete.

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

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.

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

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

Fig. 6. Effects of CD31-NP targeting in perfused human kidneys.

Fig. 4 Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after reovirus treatment. Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after.

Fig. 4. Specific versus nonspecific NP accumulation.

Fig. 5. Vascularization of human liver seed grafts.

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

Fig. 1. Aberrant JNK pathway activation in mouse models of ALS and in spinal cord tissue from patients with sporadic ALS. Aberrant JNK pathway activation.

Identification of bioactive compounds modulating STING activation

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

Type 1 immunity drives metabolic disease but protects against NAFLD

Fig. 2 In vitro assessment of hESC-RPE cell sheets.

Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.

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.

Fig. 5. Accelerated NASH-driven fibrogenesis in obese IFN-γ−/− mice is characterized by severe eosinophilic inflammation during TGF-β blockade. Accelerated.

Role of immune and inflammatory cells in lung cancer–associated PH

Fig. 7. NPs accumulate at sites of vascular obstruction.

Fig. 4. Genetically engineered PD-L1

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

Regulatory CD4+ T cell–derived IL-10 is important for B cell differentiation and the GC response. Regulatory CD4+ T cell–derived IL-10 is important for.

Fig. 7 Improvement of clinical score and axon pathology by nasal IL-4 treatment during chronic EAE. Improvement of clinical score and axon pathology by.

Fig. 4 TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV release in murine MSCs. TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV.

Fig. 1 CpG induces the expression of OX40 on CD4 T cells.

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

Inhibition of VEGFA or macrophage-specific ablation of Vegfa from TIE2hi/VEGFAhi TMEM macrophages reduces vascular permeability and tumor cell intravasation.

Fig. 3. Morphological changes associated with glial activation were reduced in 16-month-old APP/PS1;C3 KO mice. Morphological changes associated with glial.

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. Features of PH in LLC1 lung tumor mice.

Fig. 4 Surgery initiates a systemic inflammatory response that triggers the outgrowth of distant immunogenic tumors and can be inhibited by perioperative.

Fig. 1 CSPG4 is expressed in GBM specimens and GBM-NS and associated with more aggressive disease. CSPG4 is expressed in GBM specimens and GBM-NS and associated.

Fig. 4. Acute lung injury in miR-223−/y mice.

Fig. 3 CSF1 is expressed in human melanoma.

Fig. 1 Characterization of hESC-RPE cells.

Fig. 6 Photoreceptor cell survival in the RCS rat retina after transplantation with hESC-RPE cell sheets. Photoreceptor cell survival in the RCS rat retina.

Protection from autoimmunity is not due to the expansion of Treg subsets. Protection from autoimmunity is not due to the expansion of Treg subsets. (A.

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.

Correlation of reovirus RNA/protein with proliferating tumor cells

Fig. 2 CD32+ cells have a distinctively different phenotype compared to CD32− cells. CD32+ cells have a distinctively different phenotype compared to CD32−

Fig. 2. BET inhibition enhances PARPi-induced DNA damage.

Murine gingival MSCs and skin MSCs produce and secrete IL-1RA–EV

PD-L1 selectively marks circulating NCMs.

Socs1 KD tumors exhibit a more T-cell–inflamed phenotype and increased T-cell activation. Socs1 KD tumors exhibit a more T-cell–inflamed phenotype and.

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. 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.

Inflammation Mediated by JNK in Myeloid Cells Promotes the Development of Hepatitis and Hepatocellular Carcinoma Myoung Sook Han, Tamera Barrett, Michael.

CDN–treated MOC1 tumors demonstrate enhanced activation of innate and antigen-specific adaptive immunity. CDN–treated MOC1 tumors demonstrate enhanced.

HMQ1611 inhibited breast tumor growth in mice.

Intratumoral changes in critical lymphocyte populations and numbers after NKTR-214 treatment. Intratumoral changes in critical lymphocyte populations and.

Hypoxic Ag-specific CD8+ T cells are less functional and less proliferative. Hypoxic Ag-specific CD8+ T cells are less functional and less proliferative.

Anti-CD40 activates TAMs and recruits inflammatory monocytes.

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

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.

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.

PEGPH20 depletes HA and decompresses intratumoral vessels.

Presentation transcript:

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 in a CCR7-dependent manner. (A to D) B16-OVA and B16-OVA/VC tumor–bearing mice were treated with control (Iso) or VEGFR-3–blocking antibodies (αR3) starting on the day of inoculation, and tumors were characterized on day 9 by flow cytometry (data represent two independent experiments, n = 5 each). (A) Quantification of tumor-infiltrating conventional CD4+ T cells (conv CD4+; FoxP3−) and CD8+ T cells. (B) Activation status of CD4+ (top) and CD8+ (bottom) T cells. Naïve, CD44−CD62L+; effector/effector memory (EM), CD44+CD62L−; central memory (CM), CD44+CD62L+. (C) Ratio of naïve/EM in infiltrating CD4+ and CD8+ T cells. (D) CCL21 concentration as assessed by enzyme-linked immunosorbent assay (ELISA) in the tumor, dLNs, and ndLNs. (E) Representative image of a lymphangiogenic B16/VC tumor section immunostained for CD4+ T cells (red), CCL21 (green), LECs (Lyve-1, white), and DAPI (blue). Scale bar, 100 μm. (F) Quantification of CCR7+ T cell subsets in untreated B16-OVA and B16-OVA/VC tumors after 14 days (n ≥ 4). (G to J) B16-OVA/VC tumor–bearing mice were treated with Iso or anti-CCR7 (αCCR7)–blocking antibodies on days 0, 3, and 6, and (G to I) tumors were characterized on day 9 by flow cytometry or (J) mice were given adoptive transfer of 106 naïve OT-I CD8+ T cells (n ≥ 6). (G) Representative flow cytometry plots of T cell activation status. (H) Quantification of naïve and CM fractions of conventional CD4+ (left) and CD8+ (right) T cells. (I) Ratio of naïve/EM subsets. (J) Quantification of intratumoral OT-I cells as percentage of overall CD8+ T cells on day 10 after inoculation. *P < 0.05, **P < 0.01, ***P < 0.001 performed with two-tailed Student’s t test or one-way analysis of variance (ANOVA). Manuel Fankhauser et al., Sci Transl Med 2017;9:eaal4712 Published by AAAS