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Transcription profiles of fate mapped IL17aiCre+flox/stop/flox-YFP+ TH17 cells, CD44intCD27+ TH17 cells and CD44hiCD27- TH17 cells from WT or Raptor-ko (flox/flox) mice after immunization with Myelin Oligodendrocyte Glycoprotein (MOG)

ABSTRACT: Transcription profiles of fate mapped IL17aiCre+flox/stop/flox-YFP+ TH17 cells, CD44intCD27+ TH17 cells and CD44hiCD27- TH17 cells from WT or Raptor-ko (flox/flox) mice after immunization with Myelin Oligodendrocyte Glycoprotein (MOG)

PROVIDER: PRJNA420445 | ENA |

REPOSITORIES: ENA

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Transcription profiles of fate mapped IL17aiCre+flox/stop/flox-YFP+ TH17 cells, CD44intCD27+ TH17 cells and CD44hiCD27- TH17 cells from WT or Raptor-ko (flox/flox) mice after immunization with Myelin Oligodendrocyte Glycoprotein (MOG)

Project description:Mechanisms governing memory responses in IL-17 secreting CD4+ T cells (TH17), especially in autoimmune disorders, remain poorly understood. TH17 cells play pleiotropic roles in autoimmunity and tissue inflammation and are characterized by inherent plasticity, although how plasticity is regulated remains elusive. We investigated the transcriptional profiles of fate mapped (IL17aiCre-flox/stop/flox-YFP) TH17 cells and WT and Raptor-ko (flox/flox) TH17 cells (both IL17aiCre-flox/stop/flox-YFP) as well as sorted within CD27+ and CD27- subsets of WT in experimental autoimmune encephalomyelitis, a human model for human multiple sclerosis. We used microarrays to compare the global transcription profiles of YFP+ (IL17aiCre-flox/stop/flox-YFP) fate mapped TH17 cells as well as CD27+ and CD27- subsets of CD44+ fate mapped TH17 cells from draining lymph nodes on day 9 after immunization with Myelin oligodendrocyte glycoprotein from WT and IL17aCre-Raptor-flox/flox mice.

2019-03-20 | GSE107521 | GEO

Gene expression analysis of WT Th17 versus STAT4 deficient Th17 cells from EAE mice

Project description:The purpose of this study is to compare transcriptional profiles of WT and STAT4-deficient Th17 cultured cells from mice with experimental autoimmune encephalomyelitis (EAE) using RNA sequencing. WT and STAT4 deficient splenocytes from EAE immunized mice were cultured with MOG peptide under Th17 conditions for three days, and then total RNA was extracted from CD4 T cells for sequencing. Differential gene expression was determined using the DESeq2 algorithm. These data reveal a previously unrecognized role for STAT4 in Th17 gene expression and function.

2023-03-30 | GSE227049 | GEO

MOG-encoding DNA vaccines ameliorate EAE and display neuroprotective effects in treated mice summary

Project description:Vaccination with naked DNA encoding myelin basic protein represents a promising therapeutic strategy in multiple sclerosis (MS). In this study, we assessed the potential of vaccination with a DNA construct coding for the myelin oligodendrocyte glycoprotein (MOG), an important candidate autoantigen in MS, to induce tolerance and protect against experimental autoimmune encephalomyelitis (EAE). Herein, we demonstrated that MOG-DNA vaccination reduced the clinical and histopathological signs of EAE when administered in both prophylactic and therapeutic settings. Further mechanistic experiments revealed that the protective effects of MOG-DNA vaccines were associated with a reduction of antigen-specific Th1 and Th17 cellular immune responses and expansion of regulatory T cells in periphery, and up-regulation in the central nervous system of genes encoding neurotrophic factors and proteins involved in remyelination. These results may set the rationale for the use of MOG-based DNA vaccines to induce tolerance in MS patients. We analyzed brain and spinal cord samples from five treated and five control mice

2011-07-08 | E-GEOD-30482 | biostudies-arrayexpress

MOG-encoding DNA vaccines ameliorate EAE and display neuroprotective effects in treated mice summary

2011-07-08 | GSE30482 | GEO

Mouse Th17 cells

Project description:Th17 cells transcriptome

| PRJNA293472 | ENA

Mouse Th17 T cells, IL-23 stimulated

Project description:Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to characterize IL-23 signaling in primary murine Th17 cells. We quantified 6,888 phosphorylation sites in Th17 cells, and found 168 phosphorylations regulated upom IL-23 stimulation. IL-23 increased the phosphorylation of the myosin regulatory light chain (RLC), an actomyosin contractibility marker, in Th17 and Tγδ cells. IL-23-induced RLC phosphorylation required JAK2 and ROCK catalytic activity, and the study of the IL-23/ROCK axis revealed an unexpected role of IL-23 in the migration of Tγδ17 and Th17 cells. Moreover, pharmacological inhibition of ROCK reduced Tγδ17 recruitment to inflamed skin upon challenge with inflammatory agent Imiquimod. This work: i) provides new insights into phosphorylation networks that control Th17 cells, ii) widely expands the current knowledge on IL-23 signaling, and iii) contributes to the increasing list of immune cells subsets characterized by global phosphoproteomic approaches.

2020-03-25 | PXD016633 | Pride

Transcription profiles of WT and CreER-Raptor-flox/flox common myeloid progenitors (CMP), granulocyte-macrophage progenitor (GMP), or lineage negative (Lin-) stimulated with M-CSF for 12 hours

Project description:Myelopoiesis is impaired in Raptor-deleted mice (CreER-Rptor-flox/flox). To evaluate the transcriptional changes in myeloid precursors , we isolated CMP (Lin–Sca-1–c-Kit+CD34+FcγRII/IIImid), GMP (Lin–Sca-1–c-Kit+CD34+FcγRII/IIIhigh) and Lin (B220, Ly6C, Ly6G, CD3, Ter-119) negative cells (Lin–) from bone marrow of WT or CreER-Rptor-flox/flox mice. RNA was isolated from CMP and GMP immediately after sorting and Lin- cells were cultured for 12 hours with M-CSF (10 ng/mL) in 10% FBS and 1% P/S DMEM before RNA isolation. We used microarrays to compare the global transcription profiles of CMP, GMP, or Lin– stimulated with M-CSF for 12 hours from WT and CreER-Raptor-flox/flox mice.

2017-07-31 | GSE100256 | GEO

Zea mays cultivar:MoG

Project description:Zea mays MoG Exome Capture - MoG.3

| PRJNA455910 | ENA

Zea mays cultivar:MoG

Project description:Zea mays MoG Exome Capture - MoG.2

| PRJNA456569 | ENA

MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression

Project description:We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway. two biological replicates of miR-155-/- CD4+ IL-17F RFP+ T cells compared to two biological replicates of miR-155+/+CD4+IL-17F RFP+ T cells (as a control).

2013-05-01 | E-GEOD-45122 | biostudies-arrayexpress

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