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Molecular markers in the CSF proteome differentiate neuroinflammatory diseases

ABSTRACT: Manuscript "Molecular markers in the CSF proteome differentiate neuroinflammatory diseases" by Maria L. Elkjaer Arkadiusz Nawrocki, Tim Kacprowski, Anja Hviid Simonsen, Romain Marignier, Tobias Sejbaek, Helle H. Nielsen, Lene Wermuth, Peter Høgh, Finn Sellebjerg, Richard Reynolds, Jan Baumbach, Martin R. Larssen, Zsolt Illes (prepared for submission)

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cerebrospinal Fluid

SUBMITTER: Arkadiusz Nawrocki

LAB HEAD: Martin Røssel Larsen

PROVIDER: PXD017643 | Pride | 2021-02-22

REPOSITORIES: Pride

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	QHF2221.raw	Raw
	QHF2222.raw	Raw
	QHF2223.raw	Raw
	QHF2224.raw	Raw
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Publications

CSF proteome in multiple sclerosis subtypes related to brain lesion transcriptomes.

Elkjaer Maria L ML Nawrocki Arkadiusz A Kacprowski Tim T Lassen Pernille P Simonsen Anja Hviid AH Marignier Romain R Sejbaek Tobias T Nielsen Helle H HH Wermuth Lene L Rashid Alyaa Yakut AY Høgh Peter P Sellebjerg Finn F Reynolds Richard R Baumbach Jan J Larsen Martin R MR Illes Zsolt Z

Scientific reports 20210218 1

To identify markers in the CSF of multiple sclerosis (MS) subtypes, we used a two-step proteomic approach: (i) Discovery proteomics compared 169 pooled CSF from MS subtypes and inflammatory/degenerative CNS diseases (NMO spectrum and Alzheimer disease) and healthy controls. (ii) Next, 299 proteins selected by comprehensive statistics were quantified in 170 individual CSF samples. (iii) Genes of the identified proteins were also screened among transcripts in 73 MS brain lesions compared to 25 con ...[more]

PMID: 33603109

Similar Datasets

Molecular markers in the CSF proteome differentiate neuroinflammatory diseases

Project description:Manuscript "Molecular markers in the CSF proteome differentiate neuroinflammatory diseases" by Maria L. Elkjaer Arkadiusz Nawrocki, Tim Kacprowski, Anja Hviid Simonsen, Romain Marignier, Tobias Sejbaek, Helle H. Nielsen, Lene Wermuth, Peter Høgh, Finn Sellebjerg, Richard Reynolds, Jan Baumbach, Martin R. Larssen, Zsolt Illes (prepared for submission). Validation of differences in protein abundance, found in the discovery phase of the project (comparison of pools of respective samples), by analysis of proteomes of individual samples enrolled.

2022-08-08 | PXD017681 | Pride

MicroRNA profiles of 110 primary breast cancer tumors of systemically untreated, lymph node negative and estrogen receptor positive patients

Project description:MicroRNA profiles of 110 primary breast cancer tumors of systematically untreated, lymph node negative and ER positive patients. Half of the patients developed metastasis while 55 patients remained metastasis-free. The miRCURY LNA microRNA array ready-to-spot probe-set was purchased from Exiqon. The set contains capture-probes for 1212 human, 1040 mouse and 679 rat miRNAs based on the miRBase version 16. Probes were spotted in triplets on CodeLink HD (SurModics) activated glass slides and post-processed according to the CodeLink protocol. SUBMITTER_CITATION: Ines Block, Mark Burton, Kristina P. Sørensen, Lars Andersen, Martin J. Larsen, Martin Bak, Søren Cold, Mads Thomassen, Qihua Tan, Torben A. Kruse. Association of miR-548c-5p, miR-7-5p, miR-210-3p, miR-128-3p with recurrence in systemically untreated breast cancer. Oncotarget 2018 Jan; 9:9030-9042. https://doi.org/10.18632/oncotarget.24088

2018-02-16 | GSE103161 | GEO

Next Generation Sequencing of Transcriptomes of WT and Transgenic Treg cells to differentiate effect of TIM-3 on Tregulatory cell geneexpression.

Project description:Significant differences were found in transcriptional profiles of WT and TIM-3+(GFPHi and GFP Low) cells, suggesting major shifts in metabolic status, cytokine profiles and suppresive capacity of Tregulatory cells due to expression of TIM-3 in Tregulatory cells.

2021-08-16 | GSE155825 | GEO

3' RNA-seq of flies over-expressing cabut protein or RNAi against cabut mRNA

Project description:CbtOE (Tim-gal4; UAS-cbtFLAG), Tim-gal4 (control for CbtOE), cbtRNAi (Tim-gal4-UAS-Dcr2-UAS-cbtIR-cbtE1) and Tim-gal4;UAS-Dcr2 (control for CbtRNAi) flies. Flies were entrained in LD (light: dark) condition for 3-4 days and harvested at six time points: ZT3, ZT7, ZT11, ZT15, ZT19, ZT23 Fly heads were collected, RNA was extracted and RNA-seq libraries were prepared as previously described (Engreitz et al., 2013) Three samples of cbtRNAi and three samples of their controls. Two samples of cbtOE with two samples of their controls.

2015-05-08 | E-GEOD-67590 | biostudies-arrayexpress

microRNA expression in Tim-3 knockdown RAW264.7 cell

Project description:RAW264.7 cell was stably transfected with Tim-3 siRNA(SI) or negative control(NC) and were analyzed for microRNA expression Differerently expressed microRNA in Tim-3 knockdown RAW264.7 cells were summarized and were used for further analysis RAW264.7 cells stably transfected with Tim-3 siRNA(SI) or negative control(NC) and were used to collect microRNA without any other treatment

2016-01-14 | E-GEOD-76839 | biostudies-arrayexpress

Transcription profiling of mouse IgE/antigen-activated mast cells stimulated with TIM-3

Project description:TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight). Experiment Overall Design: Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments.

2009-10-15 | E-GEOD-14438 | biostudies-arrayexpress

Gene expression profile for naïve CD4+ T cells after 60-hour-treatment by IL-27

Project description:The inhibitory receptor Tim-3 has emerged as a critical regulator of the T cell dysfunction that develops in chronic viral infections and cancers. However, little is known regarding the signaling pathways that drive Tim-3 expression. Here, we demonstrate that IL-27 induces NFIL3, which promotes permissive chromatin remodeling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. We further show that the IL-27/NFIL3 signaling axis is crucial for the induction of Tim-3 in vivo. IL-27-conditioned Th1 cells exhibit reduced effector function and are poor mediators of intestinal inflammation. This inhibitory effect is NFIL3 dependent. In contrast, tumor-infiltrating lymphocytes (TILs) from IL-27R-/- mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumor growth control. Thus, our data identify an IL-27/NFIL3 signaling axis as a key regulator of effector T cell responses via induction of Tim-3, IL-10, and T cell dysfunction. Through gene expression profile analysis, we identified a series of transcription factors that are induced by IL-27. Particularly, the induction of NFIL3 is highly relevant to Tim-3 expression. Naïve CD4+ T cells from C57BL/6 mice were stimulated with plate-bound anti-CD3 and anti-CD28 antibodies for 60 hours. The cells were subjected to gene profile analysis. A comparative transcriptome analysis between cells under neutral culture condition (Untreated) and cells treated with IL-27 (IL-27-treated) was peformed to screen transcription factors that are induced by IL-27 signaling.

2015-01-31 | E-GEOD-63628 | biostudies-arrayexpress

Project description:Purple Martin (Progne subis) sequencing

| PRJNA772931 | ENA

Gene expression change induced by TIM-3/galectin-9 interaction in primary AML

Project description:Analysis of gene expression change after galectin-9 stimulation in primary CD34+TIM-3+ AML cells Total RNA obtained from purified CD34+TIM-3+ primary AML cells with or without recombinant human galectin-9 stimulation (20hrs) was subjected to transcriptome analysis

2014-10-10 | E-GEOD-62223 | biostudies-arrayexpress

Autophagic adaptation to oxidative stress alters peritoneal residential macrophage survival and ovarian cancer metastasis [macrophages]

Project description:Tumor-associated macrophages (TAMs) affect cancer progression and therapy. Ovarian carcinoma often metastasizes to the peritoneal cavity. Here, we found two peritoneal macrophage subsets in mice bearing ID8 ovarian cancer based on the Tim-4 (T-cell immunoglobulin and mucin domain containing 4) expression. Tim-4+ TAMs were embryonically originated and locally sustained while Tim-4- TAMs were replenished from circulating monocytes. Tim-4+ TAMs, but not Tim-4- TAMs, promoted tumor growth in vivo. Relative to Tim-4- TAMs, Tim-4+ TAMs manifested high oxidative phosphorylation and adapted mitophagy to alleviate oxidative stress. High levels of arginase-1 in Tim-4+ TAMs contributed to potent mitophagy activities via weakened mTORC1 activation due to low arginine resultant from arginase-1-mediated metabolism. Furthermore, genetic deficiency of autophagy element FIP200 resulted in Tim-4+ TAM loss via ROS-mediated apoptosis, and elevated T cell-immunity and ID8 tumor inhibition in vivo. Moreover, human ovarian cancer-associated CRIg (complement receptor of the Immunoglobulin superfamily) positive macrophages were transcriptionally, metabolically, and functionally similar to murine Tim-4+ TAMs. Thus, targeting CRIg+ (Tim-4+) TAMs may potentially treat ovarian cancer patients with peritoneal metastasis.

2020-09-09 | GSE157673 | GEO