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Quantitative proteomic characterization and comparison of T helper 17 and iTreg cells in mouse

ABSTRACT: Using mass spectrometry-based label free quantitative proteomics analysis of in vitro differentiated murine Th17 and induced T regulatory (iTreg) cells. More than 4000 proteins covering almost all subcellular compartments were detected. Quantitative comparison of the protein expression profiles resulted in the identification of proteins specifically expressed in the Th17 and iTreg cells. Importantly, our combined analysis of proteome and gene expression data revealed protein expression changes that were not associated with changes at the transcriptional level.

OTHER RELATED OMICS DATASETS IN: PRJNA411825

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Primary Cell, T Cell

SUBMITTER: Imran ahammad Mohammad

LAB HEAD: Zhi Jane Chen

PROVIDER: PXD007826 | Pride | 2018-06-05

REPOSITORIES: Pride

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Quantitative proteomic characterization and comparison of T helper 17 and induced regulatory T cells.

Mohammad Imran I Nousiainen Kari K Bhosale Santosh D SD Starskaia Inna I Moulder Robert R Rokka Anne A Cheng Fang F Mohanasundaram Ponnuswamy P Eriksson John E JE Goodlett David R DR Lähdesmäki Harri H Chen Zhi Z

PLoS biology 20180531 5

The transcriptional network and protein regulators that govern T helper 17 (Th17) cell differentiation have been studied extensively using advanced genomic approaches. For a better understanding of these biological processes, we have moved a step forward, from gene- to protein-level characterization of Th17 cells. Mass spectrometry-based label-free quantitative (LFQ) proteomics analysis were made of in vitro differentiated murine Th17 and induced regulatory T (iTreg) cells. More than 4,000 prote ...[more]

PMID: 29851958

Similar Datasets

Quantitative proteomic characterization and comparison of T helper 17 and iTreg cells

Project description:Using mass spectrometry-based label-free quantitative (LFQ) proteomics analysis of in vitro differentiated murine Th17 and induced T regulatory (iTreg) cells. More than 4000 proteins covering almost all subcellular compartments were detected. Quantitative comparison of the protein expression profiles resulted in the identification of proteins specifically expressed in the Th17 and iTreg cells. Importantly, our combined analysis of proteome and gene expression data revealed protein expression changes that were not associated with changes at the transcriptional level.

2018-05-31 | GSE104152 | GEO

Retinal pigment epithelial cells suppress interleukin-17-producing T-helper 17 cells

Project description:T cells that encounter cultured ocular pigment epithelial cells in vitro are inhibited from undergoing T cell receptor-triggered activation. Because retinal pigment epithelial (RPE) cells are able to suppress T-cell activation, we studied whether RPE cells could suppress cytokine production by activated T helper (Th) cells. In this study we showed that primary cultured RPE cells greatly suppressed activation of bystander CD4+ T cells in vitro, especially the cytokine production by the target T helper cells (Th1 cells, Th2 cells, Th17 cells, but not Th3 cells). Cultured RPE cells and RPE-supernatants significantly suppressed IL-17 producing CD4+ T cells, and RPE cells fully suppressed polarized Th17 cell lines that induced by recombinant proteins, IL-6 and TGFb2. Moreover, RPE cells failed to suppress IL-17 producing T cells in the presence of rIL-6. In addition, Th17 cells exposed to RPE were suppressed via TGFb, which produce RPE cells. These results indicate that retinal PE cells have immunosuppressive capacity in order to inhibit Th17-type effector T cells. Thus, ocular resident cells play a role in establishing immune regulation in the eye. Retinal pigment epithelium suppresses Th17 cells

2012-07-11 | E-GEOD-22877 | biostudies-arrayexpress

Retinal pigment epithelial cells suppress interleukin-17-producing T-helper 17 cells

2012-07-12 | GSE22877 | GEO

Interleukin-23-induced transcription factor Blimp1 promotes pathogenicity of T helper 17 cells

Project description:Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory function of Th17 cells. In contrast to thymic deletion of Blimp-1, which causes T cell development defects and spontaneous autoimmunity, peripheral deletion of this transcription factor resulted in reduced Th17 activation and reduced severity of autoimmune encephalomyelitis. Furthermore, genome wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORÎ³t, STAT-3 and p300 at the Il23r, Il17a/f and Csf2 cytokine loci to enhance their expression. Blimp-1 also directly bound to and repressed cytokine loci Il2 and Bcl6. Taken together, our results demonstrate that Blimp-1 is an essential transcription factor downstream of IL-23 that acts in concert with RORÎ³t to activate the Th17 inflammatory program. Genome-wide binding analysis of Blimp1 from in vitro generated T effector and regulatory cells

2016-06-15 | E-GEOD-75724 | biostudies-arrayexpress

RNA-seq of in vitro-generated murine T helper 17 cells

Project description:T helper (Th) 17 cells form a T cell subset which is crucial to maintain immunity against extracellular bacteria and fungi at epithelial barriers, but Th17 cells are also enriched at sites of inflammation in autoimmune disease. These sites are commonly characterised by adverse environmental conditions which are prone to trigger an ER (endoplasmic reticulum)-stress response. Our lab recently observed that the ER-stress response can be a strong driving force for Th17 cell differentiation. The aim of this RNA-seq project was to characterise the novel Th17 cell population generated by IL-6 and cyclopiazonic acid (CPA)-induced ER stress by transcriptional profiling of ER-stress generated and conventional Th17 cells. For this purpose nave IL17A-Cre Rosa-RFP CD4 T cells were cultured with a combination of Interleukin 6 with Transforming growth factor (TGF) or CPA for three days. Then, RFP-positive Th17 cells from four different experiments were enriched for by FACS sorting. Following RNA isolation using QIAGEN's RNA Mini Plus Kit and rRNA depletion accomplished with the NEBNext rRNA Depletion Kit, RNA-seq libraries were generated using the undirectional NEBNext Ultra RNA Library Prep Kit for Illumina. The libraries were sequenced as 75bp paired-end reads on a NextSeq 500 sequencer and analysed using QIAGEN's Biomedical Workbench.

2017-06-14 | E-MTAB-5692 | biostudies-arrayexpress

Quantitative measurements of ceramides and glycosphingolipids in Th17 and iTreg cells (part-II)

Project description:Part 2/5: It includes quantitative targeted measurements of sphingolipids (ceramides and glycosphingolipids) in Th17, iTreg, and their paired controls (Th0 cells).

2021-01-31 | ST001675 | MetabolomicsWorkbench

Regulation of pathogenic T helper 17 cell differentiation by steroid receptor coactivator-3

Project description:T helper 17 (Th17) cell development is programmed by the orphan nuclear receptor RORgt, but the underlying mechanism is not well understood. Nuclear receptor-mediated transcriptional activation depends on coactivators. Here we show that the steroid receptor coactivator-3 (SRC-3) critically regulates Th17 cell differentiation. Reduced incidence of experimental autoimmune encephalitis (EAE) associated with decreased Th17 cell generation in vivo was observed in mice with SRC-3 deletion specifically in T cells. In vitro, SRC-3 deficiency did not affect TGF-/IL-6-induced Th17 cell generation but severely impaired pathogenic Th17 differentiation induced by IL-1/IL-6/IL-23. Microarrays were used to showed that SRC-3 not only regulates IL-17A but also IL-1R1 expression. SRC-3 bound to Il17a and Il1r1 loci in a RORtdependent manner and was required for recruitment of the p300 acetyltransferase. Thus, SRC-3 is critical in RORt-dependent gene expression during Th17 cell-driven autoimmune diseases.

2018-05-02 | GSE113927 | GEO

Interleukin-23-induced transcription factor Blimp1 promotes pathogenicity of T helper 17 cells

Project description:Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory function of Th17 cells. In contrast to thymic deletion of Blimp-1, which causes T cell development defects and spontaneous autoimmunity, peripheral deletion of this transcription factor resulted in reduced Th17 activation and reduced severity of autoimmune encephalomyelitis. Furthermore, genome wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORγt, STAT-3 and p300 at the Il23r, Il17a/f and Csf2 cytokine loci to enhance their expression. Blimp-1 also directly bound to and repressed cytokine loci Il2 and Bcl6. Taken together, our results demonstrate that Blimp-1 is an essential transcription factor downstream of IL-23 that acts in concert with RORγt to activate the Th17 inflammatory program.

2016-06-15 | GSE75724 | GEO

Lipidomic analysis of CD4+ T-cell subsets (Th1,Th2,Th17 and iTreg cells) (part I)

Project description:Part 1/5: It includes lipidomic analysis of CD4+ T-cell subsets(Th1,Th2,Th17 and iTreg cells)and their paired controls(Th0 cells).

2021-01-28 | ST001676 | MetabolomicsWorkbench

Glycolysis Promotes Phosphoinositide 3-Kinase Signaling In Support of T Helper 17 Cell-Mediated Autoimmunity

Project description:T helper (Th) cell differentiation is driven by antigen and accessory signals that activate phosphoinositide 3-kinase (PI3K) to induce transcriptional and metabolic reprogramming including aerobic glycolysis (the Warburg effect). Here, we show that ATP generated through glycolysis fuels PI3K signaling to promote pathogenic Th17 cell responses. Mice with T cell-specific ablation of the glycolytic enzyme lactate dehydrogenase A (LDHA) were resistant to Th17 cell-mediated experimental autoimmune encephalomyelitis in association with defective T cell activation, migration, proliferation, and differentiation. LDHA deficiency crippled the cellular redox balance and inhibited ATP production causing attenuated phosphoinositide (3,4,5)-trisphosphate generation, and diminished activation of the Akt kinase and phosphorylation of its transcription factor target Foxo1. Th17 cell-specific expression of an Akt-insensitive Foxo1 mutant recapitulated the Th17 cell differentiation defects caused by LDHA deficiency. Thus, PI3K signaling and glycolytic bioenergetics constitute a positive feedback regulatory circuit essential for Th17 cell-mediated autoimmunity.

2021-03-27 | GSE164959 | GEO

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