Expression levels of genes of in vitro generated Th1 and Th17 cells from OT-II and OT-II x NKG2D-/- mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE143522 | GEO | 2020/05/15
REPOSITORIES: GEO
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Project description:Expression levels of genes of in vitro generated Th1 and Th17 cells from OT-II and OT-II x NKG2D-/- mice
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Project description:There is evidence that microglia interact with infiltrating Th1 and Th17 cells and this interaction results in mutual activation. However, the potential of a distinct cytokine milieu generated by these effector T cell subsets to activate microglia is poorly understood. In this study, we tested the ability of factors secreted by Th1 and Th17 cells to induce microglial activation. Interestingly, we found that only Th1-associated factors had the potential to activate microglia while the Th17-associated factors as well as direct contact of Th17 cells with microglia only had a minimal effect. Further Th1-derived factors triggered a proinflammatory M1-type gene expression profile in microglia Microglia harvested from mixed glial cultures were treated with supernatants from Th1- or Th17 cultures. Microglia cultured in medium was used as controls. At 16h post treatment RNA was isolated from the microglia and probed on Agilent´s murine 4x44k microarrays. RNA isolated from four independent experiments were used for the gene expression profiling. Microglia, Th1, Th17
2013-12-31 | E-GEOD-45384 | biostudies-arrayexpress
Project description:This is to compare the gene expression profile of Th1 and Th17 cells. Experiment Overall Design: Two replicates (rep1, rep2) in two groups (Th1, Th17).
2009-01-31 | E-GEOD-14026 | biostudies-arrayexpress
Project description:There is evidence that microglia interact with infiltrating Th1 and Th17 cells and this interaction results in mutual activation. However, the potential of a distinct cytokine milieu generated by these effector T cell subsets to activate microglia is poorly understood. In this study, we tested the ability of factors secreted by Th1 and Th17 cells to induce microglial activation. Interestingly, we found that only Th1-associated factors had the potential to activate microglia while the Th17-associated factors as well as direct contact of Th17 cells with microglia only had a minimal effect. Further Th1-derived factors triggered a proinflammatory M1-type gene expression profile in microglia
2013-12-31 | GSE45384 | GEO
Project description:We analyzed the transcriptome differences of BCL6-sufficient (CD4-Cre) and -insufficient (CD4-CrexBcl6fl/+) OT-II TFH cells. CD4-CrexBcl6fl/+ or control CD4-Cre OT-II T cells were transferred into CD45.1 Sap-/- mice. At day 3 post NP-OVA immunization, CXCR5hiPD-1hi TFH cells were sort-purified from the draining lymph node and prepared for RNA-seq analysis. Two technical repeats of ~200 cells per sample from each of 3 mice were included. BCL6-insufficient TFH cells differentially expressed many genes; among those downregulated were Stim1 and Plcg1, which code for STIM1 and PLCg1, respectively, that both impinge on calcium signaling downstream of TCR activation. Moreover, KEGG pathway analyses revealed that the calcium signaling-related pathway was generally upregulated in wildtype as compared to BCL6-insufficient TFH cells. These data support the notion that BCL6 control follicular T-B interactions by regulating multiple target genes involved in antigen-triggered calcium signaling in T cells.
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Project description:Transcriptome analysis to investigate the expression profile of Th0, Th1 and Th17.
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Project description:CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed. IFN-gamma+ Th1 cells from IFNgeYFP reporter mouse; comparing dnRARa to WT
2015-03-10 | E-GEOD-60354 | biostudies-arrayexpress
Project description:CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed. Identification of RARa binding in wild-type Th1 cells and mapping of enhancers using chromatin IP against p300, H3k4me1, H3k4me3, and H3k27ac in wild-type and dnRara Th1 cells.
2015-03-10 | E-GEOD-60353 | biostudies-arrayexpress
Project description:Th17 cells exhibit superior stemness and differentiation capabilities. Under specific conditions, they can be induced to differentiate into various subtypes. Here we reported that Th17-derived Th1 cells, when compared to conventional Th1 and Th17 cells, manifest less exhausted phenotype and enhanced anti-tumor activity.
2024-06-01 | GSE244717 | GEO
Project description:Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.
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