MCJ-KO microbiota transplantation to GF mice and DSS-induced colitis
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ABSTRACT:
PROVIDER: PRJEB43544 | ENA |
REPOSITORIES: ENA
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Project description:Dysbiosis plus DSS induced colitis in MCJ-KO mice model
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Project description:Metabolism of chimeric antigen receptor (CAR) T cells is emerging as an important area to improve CAR-T cell therapy in cancer treatment. Mitochondrial respiration is essential for survival and function of CAR-T cells, but developing strategies to specifically enhance mitochondrial respiration has been challenging. Here we identify MCJ/DnaJC15, an endogenous negative regulator of mitochondrial Complex I, as a metabolic target to enhance mitochondrial respiration in CD8 CAR-T cells. Loss of MCJ in CD8 CAR-T cells increases their in vitro and in vivo efficacy against mouse B cell leukemias. MCJ deficiency in TCR- specific CD8 cells also increases their efficacy against solid tumors in vivo. Furthermore, we reveal that human CD8 cells express MCJ and that silencing MCJ expression increases mitochondrial metabolism and anti-tumor activity of human CAR-T cells. Thus, we demonstrate the unique therapeutic potential of targeting MCJ to enhance the metabolism and efficacy of adoptive T cell therapies.
2024-05-02 | GSE263259 | GEO
Project description:MCJ defiency chronic model of UC
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Project description:MCJ deficient mice gut metagenome
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Project description:To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression. The DSS-treated colons derived from WT (n=3) and STAP-2 KO (n=3) mice were examined. Each strain was run in biological duplicate.
2014-04-17 | E-GEOD-48543 | biostudies-arrayexpress
Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days
2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress
Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing.
2009-05-08 | GSE15955 | GEO
Project description:RAW264.7 cells were untreated or treated with CpG+/-Gf for 6 hours. Total RNA was analyzed via Illumina Mouse Ref-8 V2. CpG‐induced genes and their regulation by Gf were examined.
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