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Transcription profiling of mouse CD4+ T cells responding to transient or persistent antigen presented by dendritic cells in vivo

ABSTRACT: These experiments were done to compare the gene expression profiles in CD4+ T cells responding to antigen presented by dendritic cells transiently or persistently. Some treatments include the activation of the dendritic cells by CD40 engagement. Experiment Overall Design: 2-4x106 lymph node cells from AND TCR-transgenic animals that expressed the congenic marker CD90.1 were transferred into double-transgenic (Ii-rTA/TIM) recipient animals that expressed the corresponding peptide from moth cytochrome c under a doxycycline-controllable promoter and were FACS-sorted 60 hours later. Recipients expressed the antigen not at all (âctrlâ), transiently (âshortâ) or throughout the experiment (âlongâ) due to different doxycycline treatment protocols. A second variable tested was the activation status of the dendritic cells: recipients were either injected by the stimulatory antibody FGK45.5 targeting CD40 (âFGKâ) or PBS (âPBSâ).

ORGANISM(S): Mus musculus

SUBMITTER: CBDM Lab

PROVIDER: E-GEOD-5245 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Profiling of CD4+ T cells responding to transient or persistent antigen presented by dendritic cells in vivo

Project description:These experiments were done to compare the gene expression profiles in CD4+ T cells responding to antigen presented by dendritic cells transiently or persistently. Some treatments include the activation of the dendritic cells by CD40 engagement. Keywords: immune response

2008-04-03 | GSE5245 | GEO

Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6). This study includes data from the spleen BALB/c mice, under steady-state or MCMV condition at different time points. 2 to 5 mice for each mouse strain for each time point were used, and were hybridized on 5 separate batches of gene chips.

2015-04-24 | E-GEOD-62729 | biostudies-arrayexpress

Transcription profiling of mouse dendritic cells from the spleens of Alymphoplasia or heterozygeous littlermates (wild type) to identify TNIK/NF-kappaB2 regulated gene products.

Project description:This study aims at identifying genes that are NIK/NF-kappaB2 responsive in murine dendritic cells matured in vivo. Experiment Overall Design: This study isolated dendritic cells from the spleens of Alymphoplasia or heterozygeous littlermates (wild type). Mice were eiter not treated as a reference or treated I.P. with 25 micrograms of LPS and 100 micrograms of agonistic anti-CD40 antibody. DCs were isolated 6 hours after treatment allowing in vivo maturation via both TLR and CD40 signals. DCs from 3 mice per group were pooled. Experiment was performed in triplicate.

2008-04-06 | E-GEOD-7219 | biostudies-arrayexpress

Transcription profiling to ompare the effects of Vitamin D3 treatment of mouse bone marrow derived dendritic cells with control, untreated cells, and additional effects of maturation of either treated or control cells with LPS

Project description:This experiment is designed to compare the effects of Vitamin D3 treatment of mouse bone marrow derived dendritic cells with control, untreated cells, and additional effects of maturation of either treated or control cells with LPS.

2006-11-01 | E-MEXP-506 | biostudies-arrayexpress

Bispecific antibodies increase the therapeutic window of CD40 agonists through selective dendritic cell targeting

Project description:Therapeutic use of agonistic anti-CD40 antibodies is a potentially powerful approach for activating the immune response to eradicate tumors. However, the translation of this approach to clinical practice has been significantly restricted due to the severe dose-limiting toxicities observed in multiple clinical trials. Here, we demonstrate that conventional type-1 dendritic cells are essential for triggering antitumor immunity but not toxicity by CD40 agonists, while macrophages, platelets, and monocytes lead to the toxic events. Therefore, we designed bispecific antibodies that target CD40 activation preferentially to dendritic cells. These bispecific reagents demonstrate a superior safety profile compared to their parental CD40 monospecific antibody, while triggering potent anti-tumor activity. We suggest such cell-selective bispecific agonistic antibodies as a drug platform to bypass the dose-limiting toxicities of anti-CD40, and of additional types of agonistic antibodies used for cancer immunotherapy.

2021-12-12 | GSE184009 | GEO

NIK/NF-kappaB2 regulated gene products.

Project description:This study aims at identifying genes that are NIK/NF-kappaB2 responsive in murine dendritic cells matured in vivo. Keywords: NIK/NF-kappaB2 responsive genes in dendritic cells after TLR/CD40 signaling

2008-03-05 | GSE7219 | GEO

Zscan4 transiently reactivates early embryonic genes during the generation of induced pluripotent stem cells

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2012-01-06 | E-GEOD-31435 | biostudies-arrayexpress

Transcriptomic analysis of inter- and intra-patient variation in human iPSC cardiomyocytes: Platform for precision medicine to predict drug toxicity

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2016-08-24 | E-GEOD-83668 | biostudies-arrayexpress

MDSC exacerbate acute hepatitis, mature and loose suppressor function CD40 dependent

Project description:Myeloid-derived suppressor cells (MDSC) represent a heterogeneous population of immature myeloid cells that accumulate in blood, liver, spleen and tumors upon chronic inflammation and tumor development in patients and mice. Acute hepatitis is characterized by a fast infiltration of inflammatory cells in the liver and increased enzymatic activity at this organ that could lead into liver fibrosis and cirrhosis. We have studied the biology of hepatic MDSC in acute hepatitis. Unexpectedly, hepatic MDSC, which accumulate in the liver of mice bearing subcutaneous tumors, failed to suppress inflammatory responses upon Con A injection, but instead were responsible for exacerbating acute liver damage. Phenotypic, genetic and functional studies demonstrated rapid changes of hepatic MDSC from a suppressor phenotype into a pro-inflammatory subset as early as 3 hours after Con A injection. An increase in the expression of pro-inflammatory cytokines, costimulatory molecules such as CD80, CD86 and CD40 along with a loss of suppressor function was noticed in mice upon Con A treatment. These changes were CD40-dependent and not found in CD40-/- MDSC. Interestingly, CD40 ligation of human MDSC in vitro resulted in down-regulation of arginase I expression and suppressor function. Finally, blockade of ROS production in hepatic MDSC ameliorated hepatocyte damage suggesting that MDSC mediated toxicity was ROS dependent. We believe that these findings reflect how MDSC plasticity can be modulated to promote inflammation, opening a new path for therapies targeting innate suppressive cells in cancer patients. EL4 tumors were established in C57BL/6 mice, then mice were injected either with PBS (n=3) or 12.5mg/kg Con A (n=3). Three hours later mice were sacrificed, liver CD11b+Gr-1+ cells were sorted and samples were processed for gene expression analysis.

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Differential activation of OT-1 CD8+ T cells by CD40-activated B cells and dendritic cells

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