Selective stimulation of IL-4 receptor on smooth muscle induces airway hyper-responsiveness in mice.
Selective stimulation of IL-4 receptor on smooth muscle induces airway hyperresponsiveness in mice.
Specimen part, Treatment
View SamplesThe aim of this work was to identify genes induced by IL-9 in the colon of IL-9-tarnsgenic mice (Tg5). Therefore, we performed a comprehensive study of the genes expressed in the colon of IL-9 transgenic and wild type FVB mice, taking advantage of the affymetrix microarray technology.
IL-9 promotes IL-13-dependent paneth cell hyperplasia and up-regulation of innate immunity mediators in intestinal mucosa.
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View SamplesBmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by cytokine stimulation after 24 hrs cells were infected with mycobacterium tuberculosis to identify the host factors involved in infection.
IL-4Rα-dependent alternative activation of macrophages is not decisive for Mycobacterium tuberculosis pathology and bacterial burden in mice.
Sex, Specimen part
View SamplesGene expression of Treg cells that have lost Foxp3 expression and acquired Il4 expression following adoptive transfer into T-cell deficient mice (HpTR-IL-4gfp+), cmpared to conventional Treg cells isolated from H. polygyrus-infected wild-type mice (HpTR) and Th2 cells generated from nave T cells following adoptive transfer into H. polygyrus-infected T-cell deficient mice (nT-IL-4gfp+).
Interleukin 4 promotes the development of ex-Foxp3 Th2 cells during immunity to intestinal helminths.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Batf2/Irf1 induces inflammatory responses in classically activated macrophages, lipopolysaccharides, and mycobacterial infection.
Sex, Specimen part
View SamplesBmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by cytokine stimulation
Batf2/Irf1 induces inflammatory responses in classically activated macrophages, lipopolysaccharides, and mycobacterial infection.
Sex, Specimen part
View SamplesBmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by transfection with Batf2 ShRNA.
Batf2/Irf1 induces inflammatory responses in classically activated macrophages, lipopolysaccharides, and mycobacterial infection.
Sex, Specimen part
View SamplesIL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. Gene array analysis on Stat6 and T-bet double deficient Th17 cells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TGFbeta, and associated with Th17 IL-10 production. Both c-Maf and IL-10 induction during Th17 polarization depended on Stat3, but not Stat6 or Stat1, and mechanistically differed from IL-10 regulation by Th2 or IL-27 signals. TGFbeta was also synergistic with IL-27 to induce c-Maf, and induced Stat1 independent IL-10 expression in contrast to IL-27 alone. Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6 deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression through binding to a MARE motif in the IL-10 promoter. Together, these data reveal a novel role for c-Maf in regulating T effector development, and suggest that TGFbeta may antagonize Th17 immunity by IL-10 production through c-Maf induction.
c-Maf regulates IL-10 expression during Th17 polarization.
Sex, Specimen part
View SamplesBackground There are conflicting reports on the impact of soy on breast carcinogenesis. This study examines the effects of soy supplementation on breast cancer-related genes and pathways. Methods Women (n = 140) with early-stage breast cancer were randomized to soy protein supplementation (n = 70) or placebo (n = 70) for 7 to 30 days, from diagnosis until surgery. Adherence was determined by plasma isoflavones: genistein and daidzein. Gene expression changes were evaluated by NanoString inin pre- and post-treatment tumor tissue. Genome-wide expression analysis was performed on post-treatment tissue. Proliferation (Ki67) and apoptosis (Cas3) were assessed by immunohistochemistry. Results Plasma isoflavones rose in the soy group (two-sided Wilcoxon rank-sum test, P < .001) and did not change in the placebo group. In paired analysis of pre- and post-treatment samples, 21 genes (out of 202) showed altered expression (two-sided Students t-test, P < .05). Several genes including FANCC and UGT2A1 revealed different magnitude and direction of expression changes between the two groups (two-sided Students t-test, P < .05). A high-genistein signature consisting of 126 differentially expressed genes was identified from microarray analysis of tumors. This signature was characterized by overexpression (>2 fold) of cell cycle transcripts, including those which promote cell proliferation, such as FGFR2, E2F5, BUB1, CCNB2, MYBL2, CDK1, and CDC20 (P < .01). Soy intake did not result in statistically significant changes in Ki67 or Cas3. Conclusions Gene expression associated with soy intake and high plasma genistein define a signature characterized by overexpression of FGFR2 and genes that drive cell cycle and proliferation pathways. These findings raise the concerns that in a subset of women soy could adversely affect gene expression in breast cancer.
The effects of soy supplementation on gene expression in breast cancer: a randomized placebo-controlled study.
Treatment
View SamplesTumor associated macrophages are contributing to local invasion, angiogensis, and metastasis during the progression of many kinds of tumor including glioma
Oligodendrocyte progenitor cells promote neovascularization in glioma by disrupting the blood-brain barrier.
Specimen part
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