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The role of TIGIT in idiopathic inflammatory myopathies

ABSTRACT: The role of TIGIT in idiopathic inflammatory myopathies

PROVIDER: PRJNA1148962 | ENA |

REPOSITORIES: ENA

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The role of TIGIT in idiopathic inflammatory myopathies

Project description:To investigate the role of Tight in idiopathic inflammatory myopathies.We evaluated global transcriptome changes in the quadriceps muscles of Tight-/- and WT mice with EAE. For EAM induction, 6-week-old female BALB/c mice were immunized with 100 μl of 50% complete Freund’s adjuvant (Sigma, USA) containing 1mg myosin (or with an equal volume of PBS in control group) on bilateral sides of the hind foot pads, the tail base and flanks four times at 1-week intervals as previously described.

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The characterization of circulating extracellular vesicles and small non-coding RNAs cargo in idiopathic inflammatory myopathies reveals differences across clinically diagnosed myositis subsets

Project description:Objective. To investigate the epigenetic footprint of idiopathic inflammatory myopathies (IIM) through characterization of circulating extracellular vesicles (EVs) and the expression of EV-derived small non-coding RNAs (sncRNAs).

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MicroRNA and mRNA profiling in the idiopathic inflammatory myopathies

Project description:Objectives: The idiopathic inflammatory myopathies (IIMs) are heterogeneous autoimmune conditions of skeletal muscle inflammation and weakness. MicroRNAs (miRNAs) are short, non-coding RNA which regulate gene expression of target mRNAs. The aim of this study was to profile miRNA and mRNA in IIM and identify miRNA-mRNA relationships which may be relevant to disease. Materials and methods: mRNA and miRNA in whole blood samples from 7 polymyositis (PM), 7 dermatomyositis (DM), 5 inclusion body myositis (IBM) and 5 non-myositis controls was profiled using next generation RNA sequencing. Gene ontology and pathway analyses were performed using GOseq and Ingenuity Pathway Analysis. Dysregulation of miRNAs and opposite dysregulation of predicted target mRNAs in IIM subgroups was validated using RTqPCR and investigated by transfecting human skeletal muscle cells with miRNA mimic. Results Analysis of differentially expressed genes showed that interferon signalling and anti-viral response pathways were upregulated in PM and DM compared to controls. An anti-Jo1 autoantibody positive subset of PM and DM (n=5) had more significant upregulation and predicted activation of interferon signalling and highlighted T-helper (Th1 and Th2) cell pathways. In miRNA profiling miR-96-5p was significantly upregulated in PM, DM and the anti-Jo1positive subset. RTqPCR replicated miR-96-5p upregulation and predicted mRNA target (ADK, CD28 and SLC4A10) downregulation. Transfection of a human skeletal muscle cell line with miR-96-5p mimic resulted in significant downregulation of ADK. Conclusion: MiRNA and mRNA profiling identified dysregulation of interferon signalling, anti-viral response and T-helper cell pathways, and indicates a possible role for miR-96-5p regulation of ADK in pathogenesis of IIM.

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Transcription profiling of human muscle tissue in patients with inflammatory myopathies

Project description:Molecular profiles of muscle tissue in patients with inflammatory myopathies

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Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies

Project description:Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies

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Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies

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TIGIT+ Tregs

Project description:TIGIT+ Tregs suppress Th1 and Th17 responses while sparing Th2 responses. Analysis of global gene expression of TIGIT+ vs. TIGIT- Tregs from naive mice reveled that TIGIT+ Tregs display an activated phenotype and are enriched for Treg signature genes including the Treg effector molecule Fgl2 which enables them to selectively spare Th2 responses. TIGIT+ and TIGIT- Tregs were sorted from naïve Foxp3-GFP KI mice (pooled spleen and lymph nodes) TIGIT: T cell immunoreceptor with Ig and ITIM domains

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Immunoglobulin G N-glycosylation associates with novel endotypes of idiopathic inflammatory myopathies patients

Project description:Objectives: This study aimed to investigate the association between immunoglobulin G (IgG) N-glycosylation patterns and the clinical endotypes of patients with idiopathic inflammatory myopathies (IIM), potentially informing disease classification and therapeutic target identification. Methods: We recruited 168 IIM patients and 52 healthy controls, and performed IgG N-glycosylation profiling using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and employed GlycoQuant for intact glycopeptide analysis. Clinical data were extracted, and statistical analyses were conducted to correlate glycosylation profiles with clinical manifestations. Unsupervised clustering analysis was applied to identify novel IIM subgroups based on differential IgG N-glycosylation. Results: Our analysis revealed significant disparities in IgG N-glycosylation between IIM patients and controls, with 13 specific glycoforms exhibiting marked alterations. The level of fucosylated glycans was significantly higher in the IIM patients than healthy controls. Three distinct IIM endotypes were identified, each characterized by unique glycosylation signatures and clinical phenotypes. These endotypes were not congruent with conventional diagnostic subgroups and demonstrated associations with various clinical outcomes, including muscle weakness, interstitial lung disease (ILD), and serological profiles.

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