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

Slides:



Advertisements
Similar presentations
Loss of Hdac3 impairs Ar signaling in mouse prostate tissues and has no effect on apoptosis Loss of Hdac3 impairs Ar signaling in mouse prostate tissues.
Advertisements

Fig. 1. TP is highly expressed in myeloma.
Fig. 1. Loss of circadian rhythms in iKO mice.
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.
Transfer of miR-223 during neutrophil-epithelial cell interactions
Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.
Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.
Volume 20, Issue 3, Pages (July 2017)
Fig. 2 TLR8 is aberrantly expressed on pDCs from SSc patients.
Fig. 8. In vivo suppression of MM by CMLD
MRSA virulence proteins cause LMC death and diminished CLV function
Fig. 1 MT-2 ameliorates asthmatic pulmonary resistance.
Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.
Fig. 7. The PD-L1 defect is evident in HSPCs from T1D patients.
Fig. 4. The effects of AVP or d(Leu4Lys8)VP, a specific AVPR1B agonist, on anemic rodents. The effects of AVP or d(Leu4Lys8)VP, a specific AVPR1B agonist,
Fig. 5 A competent Fc is required for the antitumor immune response.
Fig. 3. Wisper controls CF behavior and survival.
Fig. 5. Stimulation of EPO expression and secretion under hypoxic culture conditions. Stimulation of EPO expression and secretion under hypoxic culture.
Fig. 3 Biological function of TG2 and the interaction with MT-2.
CHK1 downregulation upon ERG overexpression.
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.
Persistence of CAR4 cells is reduced after sustained TCR engagement
Fig. 4. Restriction of TCR antigen to hematopoietic tissues does not prevent CAR8 exhaustion and failure of leukemia clearance. Restriction of TCR antigen.
Fig. 3. Genetically engineered PD-L1
Fig. 1. mGlu7 expression is reduced in RTT autopsy samples.
Fig. 1. Neurobehavioral testing in YG8R mice transplanted with wild-type mouse HSPCs. Neurobehavioral testing in YG8R mice transplanted with wild-type.
Fig. 2. Resistance to S63845-induced apoptosis through loss of BAK or elevated BCL-XL. Resistance to S63845-induced apoptosis through loss of BAK or elevated.
Fig. 4. Genetically engineered PD-L1
Fig. 5. pKL cells abrogate the autoimmune response in vitro.
Fig. 3. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and CREB. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and.
Fig. 5 Local gel scaffold for T cell memory response.
Fig. 3. ERRα is involved in the regulation of OPLAH.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 1 BX795 suppresses HSV-1 infection.
Volume 23, Issue 4, Pages (April 2018)
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
BRAFV600E promotes glycolysis in melanoma cells via regulation of GLUT1, GLUT3, and HK2. BRAFV600E promotes glycolysis in melanoma cells via regulation.
Fig. 6. pKL cells revert hyperglycemia in NOD mice in vivo.
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.
Characterization of MET‐addicted cells rendered resistant to MET tyrosine kinase inhibitors Characterization of MET‐addicted cells rendered resistant to.
Fig. 3 Hepatic HBV envelope RNA and protein expression levels in HBVRplRag−/− mice 7 days (1 week) and 8 to 24 weeks after adoptive transfer with WT or.
Fig. 2 In vitro and preclinical study with 18F-MPG.
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.
Fig. 2 Adoptive transfer of adult Ox40−/− splenocytes into adult HBVEnvRag−/− mice alters hepatic inflammation, HBsAg clearance, HBsAb seroconversion,
Significant differences in translational efficiencies of DNA damage repair pathway genes between patient clusters. Significant differences in translational.
Fig. 4. Acute lung injury in miR-223−/y mice.
Fig. 2. Cellular response to FolamiRs in vitro.
Fig. 1. Specificity of FolamiR uptake in cancer cells in culture.
Fig. 6 DMF inhibits NF-κB translocation upon infection.
Fig. 5 Early and modest immune response at day 3 after exposure in Delayed animals. Early and modest immune response at day 3 after exposure in Delayed.
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.
Fig. 4. Induced Zbtb7a in lungs is localized to AMs.
IFN-γ antagonizes TGF-β in vivo.
Setdb1 has cell-intrinsic functions in B cell development.
Fig. 1 KCC2 down-regulation is prevented in sortilin-deficient mice.
Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.
Fig. 1. PARN is differentially expressed in breast cancer versus non-cancerous tissue/cells. PARN is differentially expressed in breast cancer versus non-cancerous.
Arginine-to-lysine mutations conferring TRIM22 restriction and lysine-to-arginine mutations causing loss of TRIM22 restriction. Arginine-to-lysine mutations.
A-E: Bcl family gene regulation in human islets cultured in high versus normal glucose. A-E: Bcl family gene regulation in human islets cultured in high.
KIF13A depletion leads to a drop in virus titers, without affecting viral protein expression. KIF13A depletion leadsto a drop in virus titers, without.
Fig. 4. Genetically engineered PD-L1
Hepatocyte Growth Factor Regulates the miR-206-HDAC4 Cascade to Control Neurogenic Muscle Atrophy following Surgical Denervation in Mice  Wooshik Choi,
CPPED1 (A) and PPARγ2 (B) mRNA expressions in cultured SGBS cells during adipocyte differentiation. CPPED1 (A) and PPARγ2 (B) mRNA expressions in cultured.
Fig. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.
Targeting p53-dependent stem cell loss for intestinal chemoprotection
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model
Presentation transcript:

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs. Mechanism of PD-L1 down-regulation in NOD HSPCs. (A) Bar graphs depicting percentage of PD-L1+ cells within KL cells isolated from bone marrow of C57BL/6 and NOD mice and cultured for 3 days in normal glucose, in 20 mM, or in 35 mM high glucose. Experiments were run in triplicate. NG, normal glucose; HG-20, 20 mM high glucose; HG-35, 35 mM high glucose. (B) Proliferation rates of carboxyfluorescein succinimidyl ester (CFSE)–labeled KL cells obtained from C57BL/6 and NOD bone marrow at baseline and after 1 and 3 days of culture. (C) Frequency of apoptosis of KL cells obtained from bone marrow of C57BL/6 and NOD mice at baseline and after 1 and 3 days of culture. For statistical analysis in (A) to (C), one-way ANOVA followed by Bonferroni multiple comparison test for group comparisons between C57BL/6 and NOD mice; in (A): P = not significant (ns); in (B): #P < 0.0001 versus all except NOD–day 0 (D0) (P = ns); in (C): §P < 0.0001 versus all except NOD-D0 (P = ns) and NOD-D1 (P < 0.001); #P < 0.0001 versus all except NOD-D1 (P = ns). 7-AAD, 7-aminoactinomycin D. (D) MA plot for GWAS performed in KLS cells obtained from bone marrow of C57BL/6 compared to NOD mice; MA-plot, log2 normalized expression levels of expression for KLS cells from C57BL/6 (y axis) in comparison with KLS cells from NOD (x axis). Avg, average. (E and F) List of miRNAs significantly up-regulated (E) and down-regulated (F) in KLS cells obtained from the bone marrow of NOD as compared to C57BL/6 mice. (G) miRNA network controlling PD-L1 gene expression generated with MGI. (H and I) KL cells obtained from bone marrow of NOD mice were cultured in the presence of miR-1905 inhibitor, and wild-type (WT) (untreated KL) were used as controls. qRT-PCR of miR-1905 (H) and qRT-PCR of PD-L1 (I) are shown. Experiments were run in triplicate, and statistical significance was determined using two-tailed unpaired Student’s t test. (J) Western blotting and quantitative bar graphs of PD-L1 protein expression in KL cells obtained from bone marrow of NOD mice cultured in the presence of miR-1905 inhibitor, and WT (untreated KL) were used as controls, with GAPDH used as an internal control. Experiments were run in triplicate, and statistical significance was determined using two-tailed unpaired Student’s t test (P = 0.0005). (K) Methylation status of the PD-L1 locus in KLS cells obtained from the bone marrow of C57BL/6 and NOD mice. Experiments were run in triplicate, and statistical significance comparing methylated CpG% of C57BL/6 to NOD was determined using two-tailed unpaired Student’s t test. Data are expressed as means ± SEM. Data are representative of at least n = 3 mice. *P < 0.05; **P < 0.01; ***P < 0.0001. Moufida Ben Nasr et al., Sci Transl Med 2017;9:eaam7543 Published by AAAS