Fig. 4. Genetically engineered PD-L1

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Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

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Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A)

Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.

Fig. 7. The PD-L1 defect is evident in HSPCs from T1D patients.

Specific depletion of TFH and LCMV-specific CD4 T cells.

VLPs activate DCs and antigen-specific CD8+ T cells via the STING and cGAS pathway. VLPs activate DCs and antigen-specific CD8+ T cells via the STING and.

CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.

CD169+ macrophages play a critical role in mediating innate immune cell reorganization. CD169+ macrophages play a critical role in mediating innate immune.

Specific depletion of CD4-DTR–derived CD4 T cells.

Fig. 3. Genetically engineered PD-L1

Fig. 4. Genetically engineered PD-L1

Fig. 5. pKL cells abrogate the autoimmune response in vitro.

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.

CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.

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.

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

Role of TLR signaling in hY4-induced changes and effects of TLR inhibition. Role of TLR signaling in hY4-induced changes and effects of TLR inhibition.

Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.

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.

Human cells produce type I and III IFNs upon Af stimulation.

Abundance of non–islet-specific CTLs at islets is immune-suppressive.

Tfr cells robustly secrete IL-10 after acute viral infection.

Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.

T-bethi MP cells produce IFN-γ in response to IL-12.

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

TCR signaling is required for exhausted-like TRM cell formation and maintenance. TCR signaling is required for exhausted-like TRM cell formation and maintenance.

Low accessibility to Ag for CTLs leads to low proliferation of effectors. Low accessibility to Ag for CTLs leads to low proliferation of effectors. Intravital.

IFN-γ antagonizes TGF-β in vivo.

Fig. 4. Peanut-specific TH2A cells are specifically targeted during immunotherapy. Peanut-specific TH2A cells are specifically targeted during immunotherapy.

Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras. Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras.

Ag governs CTL behavior at islets but is not required for their accumulation in large numbers. Ag governs CTL behavior at islets but is not required for.

Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A)

Fig. 5 Quantitative assessment of the efficacy of the tissue-engineered implant to heal the TMJ disc defect. Quantitative assessment of the efficacy of.

Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.

Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.

APCs from hypertensive mice present antigens more efficiently.

PD-1, but not PD-L1, expressed by the BDC2

High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.

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

Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.

Slc7a5 expression in preosteoclasts is reduced in ovariectomized mice.

Fig. 3 Biological function of TG2 and the interaction with MT-2.

RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.

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.

CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.

Fig. 1 Neu1−/− fibroblasts have characteristics of myofibroblasts.

Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.

Fig. 7 BMS reduces the elevated expression of type I IFN–regulated genes both ex vivo in blood from patients with lupus and in a phase 1 study of.

BMS blocks functional responses in primary immune cells driven by IFNα

Fig. 5 Treatment with BMS (PO BID) protects from wasting and colitis in two SCID mouse models. Treatment with BMS (PO BID) protects from.

Fig. 6 Caspase-3– and -7–deficient cells maintain mitochondrial membrane polarity following intrinsic or extrinsic apoptotic stimuli. Caspase-3– and -7–deficient.

Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.

Fig. 4 PD-L1 expression is found in the spleen and the BM of mice transplanted with JAK2V617F-transduced bone marrow. PD-L1 expression is found in the.

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

CD4+ memory T cells derived from either CD25hi or CD25lo effector cells respond robustly to secondary challenge. CD4+ memory T cells derived from either.

CD25 expression predicts effector and memory differentiation.

PD and efficacy of AZD4785 in KRAS mutant lung cancer xenograft models

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

Treg expression of Gata3 plays a major role in controlling dermal fibrosis. Treg expression of Gata3 plays a major role in controlling dermal fibrosis.

Chronic Treg reduction results in dermal fibrosis.

Tregs preferentially regulate TH2 cytokines in skin.

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.

Chronic Treg reduction exacerbates bleomycin-induced skin fibrosis.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 1 TLR2 expression is induced during OIS.

Fig. 6 Pharmacologic alterations of β-AR signaling regulate cardiomyocyte abscission and endowment. Pharmacologic alterations of β-AR signaling regulate.

PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model

Fig. 6 tlr2 is necessary for SASP activation in vivo.

Fig. 2 Cxxc1 deficiency restricts T cell–mediated autoimmunity and increases sensitivity to C. rodentium infection. Cxxc1 deficiency restricts T cell–mediated.

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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 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works