Fig. 4. Genetically engineered PD-L1

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Supplementary Figure 1 Supplementary Figure 1: ROR agonists increase the expression of a luciferase reporter driven by Gal4-ROR. In HEK293T cells, Gal4-ROR
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Fig. 1. TP is highly expressed in myeloma.
The gene encoding TP53INP1 is expressed in pancreatic endocrine cells A, B(A, B) Immunocytofluorescent staining of TP53INP1 (red) and insulin (green) in.
Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.
Fig. 5. Blocking LTB4 during initial lymphangiogenesis period abrogates the therapeutic benefit of LTB4 antagonism. Blocking LTB4 during initial lymphangiogenesis.
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
CD1dhiCD5+ B cells are expanded in pancreatic neoplasia and are functionally important for sustaining growth of KrasG12D-PDEC in vivo. CD1dhiCD5+ B cells.
Cytotoxic therapy induces macrophage recruitment, as well as CSF1 and IL-34 mRNA expression. Cytotoxic therapy induces macrophage recruitment, as well.
Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.
Fig. 5 Maraba induces antitumor T cell immunity.
Fig. 4. aPD-1 mAb transfer to macrophages is mediated by FcγRs.
Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.
Fig. 1 MT-2 ameliorates asthmatic pulmonary resistance.
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.
Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.
Maraba treatment sensitizes 4T1 tumors to immune checkpoint blockade
Fig. 7. The PD-L1 defect is evident in HSPCs from T1D patients.
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. 5. Stimulation of EPO expression and secretion under hypoxic culture conditions. Stimulation of EPO expression and secretion under hypoxic culture.
Blocking Activator Protein 1 Activity in Donor Cells Reduces Severity of Acute Graft- Versus-Host Disease through Reciprocal Regulation of IL-17–Producing.
Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Volume 143, Issue 1, Pages (July 2012)
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. 4. MATE1 transcription in RCC.
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. 8 TLR8 exacerbates disease in the BLM-induced fibrosis model.
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. 3. Genetically engineered PD-L1
Fig. 5. pKL cells abrogate the autoimmune response in vitro.
Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.
Fig. 5 Local gel scaffold for T cell memory response.
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Fig. 6 Alarmin release and sympathetic stress response synergize in poststroke atheroprogression. Alarmin release and sympathetic stress response synergize.
Fig. 6. pKL cells revert hyperglycemia in NOD mice in vivo.
Fig. 7. Genetic ablation of UCP2 compromised the protective effect of exogenous irisin on lung IR injury. Genetic ablation of UCP2 compromised the protective.
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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.
Volume 43, Issue 5, Pages (November 2015)
Fig. 2 Adoptive transfer of adult Ox40−/− splenocytes into adult HBVEnvRag−/− mice alters hepatic inflammation, HBsAg clearance, HBsAb seroconversion,
Fig. 4. Dabrafenib and trametinib changed the cellular components of the tumor microenvironment. Dabrafenib and trametinib changed the cellular components.
Fig. 5 DMN-Tre labeling is selective for live mycobacteria.
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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.
Volume 41, Issue 4, Pages (October 2014)
Fig. 4 The PTEN pathway in Tregs is required to suppress immune responses to apoptotic cells. The PTEN pathway in Tregs is required to suppress immune.
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PD-1, but not PD-L1, expressed by the BDC2
Fig. 4. Genetically engineered PD-L1
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The number of islet antigen–specific T cells is reduced in CT-treated RIP-LCMV-GP mice. The number of islet antigen–specific T cells is reduced in CT-treated.
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by Gonghua Huang, Yanyan Wang, Peter Vogel, and Hongbo Chi
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SY-1425 induces maturation in RARA-high AML
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Fig. 6 Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9 in vivo. Antitumor effect on tumor growth and pulmonary metastasis of CSSD-9.
The CD8+ cytotoxic T-cell response in Ron TK−/− hosts in response to tumors is necessary and sufficient to block metastasis. The CD8+ cytotoxic T-cell.
IL35 regulation of tumor growth is accompanied by suppression of CD4+ effector T-cell activity and expansion of Tregs. IL35 regulation of tumor growth.
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
Repulsive Guidance Molecule-a Is Involved in Th17-Cell-Induced Neurodegeneration in Autoimmune Encephalomyelitis  Shogo Tanabe, Toshihide Yamashita  Cell.
PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model
Fig. 5 Effects of in vivo blockade of TLR9 on adipose tissue inflammation and insulin resistance in WT mice. Effects of in vivo blockade of TLR9 on adipose.
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Fig. 4. Genetically engineered PD-L1 Fig. 4. Genetically engineered PD-L1.Tg KL cells traffic to the pancreas in hyperglycemic NOD mice. Genetically engineered PD-L1.Tg KL cells traffic to the pancreas in hyperglycemic NOD mice. (A) Insulitis score: n = 9 sections per group were analyzed. Unt, untreated. (B) OVA rechallenge test. Data are representative of one experiment performed in three mice per group, and statistical significance was determined by using two-tailed unpaired t test. Unimm Unt, unimmunized untreated; Imm Unt, immunized untreated; Imm WT, immunized treated with KL; Imm Tg, immunized treated with PD-L1.Tg KL cells. (C) Immunophenotypic analysis of lymphocytes isolated from spleens by flow cytometry of FoxP3+ regulatory T cells (Tregs) in PD-L1.Tg KL cell–treated NOD mice as compared to untreated NOD mice. Data are representative of one experiment performed in three mice per group, and statistical significance was determined by using two-tailed unpaired t test. (D) Quantification of IFN-γ–producing cells (with number of spots normalized for background) in an ex vivo assay, in which splenocytes were challenged with islet peptides [BDC2.5, IGRP, glutamic acid decarboxylase 65 (GAD-65), and insulin] 40 days after treatment in newly hyperglycemic PD-L1.Tg KL cell–treated NOD mice or in untreated hyperglycemic NOD mice. Data are expressed as means ± SEM, and statistical significance was determined by using two-tailed unpaired t test. Data are representative of at least n = 3 mice. *P < 0.05; **P < 0.01; ***P < 0.001. #P < 0.05 versus all; §P < 0.05 versus all. (E and G) Representative flow cytometric analysis and quantitative bar graphs of ZsGreen+PD-L1.Tg KL cells in the pancreas of hyperglycemic (Hyper) and normoglycemic (Normo) NOD mice at 1, 7, and 14 days after treatment with PD-L1.Tg KL cells. Experiments were run in triplicate [in (F): in duplicate], and statistical significance was determined by using two-tailed unpaired t test. (F and H) Quantification of ZsGreen mRNA in the pancreas of hyperglycemic and normoglycemic NOD mice by qRT-PCR after treatment with PD-L1.Tg KL cells. (I and K) Bar graphs depicting flow cytometric quantification of ZsGreen+PD-L1.Tg KL cells and (J and L) quantification of ZsGreen mRNA by qRT-PCR in the bone marrow of hyperglycemic and normoglycemic NOD mice, after treatment with PD-L1.Tg KL cells. Experiments were run in triplicate [in (M): in duplicate], and statistical significance was determined by using two-tailed unpaired t test. (M and O) Bar graphs for flow cytometric quantification of ZsGreen+PD-L1.Tg KL cells and (N and P) quantification of ZsGreen mRNA by qRT-PCR in the spleen of hyperglycemic and normoglycemic NOD mice. (Q and R) Confocal imaging of pancreatic sections obtained from normoglycemic or hyperglycemic NOD mice after 1, 7, and 14 days after treatment with ZsGreen+PD-L1.Tg KL cells. Histology magnification, ×63 in all confocal images. Scale bars, 5 μm. (S and T) Luminescent images of NOD mice adoptively transferred with luciferase+PD-L1.Tg KL cells after 1 and 7 days of treatment. Data are expressed as means ± SEM. Data are representative of at least n = 2 mice. Statistical significance was determined using two-tailed unpaired t test. *P < 0.05; **P < 0.01; ***P < 0.001. CTRL, control. Moufida Ben Nasr et al., Sci Transl Med 2017;9:eaam7543 Published by AAAS