Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290324 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation [Rn]
| PRJNA290323 | ENA
Project description:Rapid CLIP Dissociation from MHC II Promotes an Unusual Antigen Presentation Pathway in Autoimmunity
| PRJNA485179 | ENA
Project description:We use transcriptome analysis to study the spinal cord transcriptome during MHV-induced demyelinating disease and find important biological pathways for demyelinating pathology. We find evidence of a Th1 cytokine response, ongoing antigen presentation and lymphocyte proliferation, lipid metabolism changes, and eicosanoid inflammation. In addition, we report several genes important for osteoclast function have augmented expression in the CNS during demyelination, suggesting a parallel between the osteoclast and microglial functions in maintaining homeostasis and the fidelity of specialized extracellular matrices in their respective compartments. RNA-seq of mock-infected and MHV-infected spinal cord tissue at 33 days post-infection, the peak of demyelination.
2013-06-15 | E-GEOD-44333 | biostudies-arrayexpress
Project description:We have been interested whether peripheral tolerance can be restored by vaccination with antigen-presenting cells (APCs) loaded with apoptotic bodies. Dendritic cells (DCs) are powerful APCs that have a critical role in the initiation and progression of autoimmunity. We previously demonstrated that DCs loaded with apoptotic islet cells prevents experimental type 1 diabetes (T1D), an autoimmune disease caused by beta-cell destruction. The goal of this study is to characterize the molecular changes on gene expression -transcriptome- occurring in these DCs pulsed with apoptotic bodies. Cells from four different genetically identical NOD (Non-Obese Diabetic) mice were used to obtain DCs. DCs were loaded with apoptotic bodies from NIT-1 cell line (insulinoma from NOD mice). Unloaded DCs were used as control in four paired experiments. Moreover, transcriptome from NIT-1 apoptotic bodies was determined. Mouse Gene 1.0 ST Arrays from Affymetrix (28,853 genes) were hybridized and genes with a p-value <= 0.002, adjusted p-value <= 0.08 and fold change (FC) >= 1.38 were considered upregulated, and genes with FC <= -1.37 were considered downregulated. Results demonstrate that apoptotic cells engulfment promotes molecular changes in DCs towards tolerogenic features. Gene expression profile of DCs from NOD mice that captured NIT-1 apoptotic bodies showed a downregulation of genes involved in antigen presentation and differential expression of cytokine, chemokine, natural immunity and immunoregulation genes together with the presence of specific transcripts for islet autoantigens. Molecular changes of DCs caused by the uptake of apoptotic bodies are key factors to induce antigen-specific peripheral tolerance.
2013-05-22 | E-MEXP-3374 | biostudies-arrayexpress
Project description:Increased antigen cross-presentation but impaired cross-priming after activation of PPARγ is mediated by up-regulation of B7H1 Dendritic cells (DCs) are able to take up exogenous antigens and present antigen-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of antigen-presenting cells (APCs), has been demonstrated to target soluble antigens exclusively towards cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model antigen ovalbumin (OVA). We could demonstrate both in vitro and in vivo that activation of PPARγ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARγ in DCs induced up-regulation of the co-inhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARγ which might open new possibilities in development of therapeutical approaches aimed at the control of excessive immune responses, e.g. in T cell-mediated autoimmunity. Comparison of murine mannose receptor negative versus mannose receptor positive bone marrow-derived DCs
2010-05-08 | E-GEOD-15616 | biostudies-arrayexpress
Project description:Chronic endoplasmatic reticulum stress in myotonic dystrophy type 2 promotes autoimmunity via mitochondrial DNA release
| PRJNA1013325 | ENA
Project description:Current cancer immunotherapies are assumed to improve infiltration and cytotoxicity of immune cells in the tumor. However, tumor cells have developed a variety of resistance mechanisms to suppress the MHC class I antigen presentation, and thereby impair the cytotoxicity of CD8+ T cells. Here, we identified Mal2 as a key player that mediates the turnover of the antigen-MHC-I complex and reduce the antigen presentation on tumor cells. Mal2 promotes the endocytosis of tumor antigen via direct interaction with the MHC-I complex and endosome-associated Rab5/7. In mouse and human breast tumor models, inhibition of Mal2 profoundly enhanced the cytotoxicity of tumor-infiltrating CD8+ T cells and suppressed breast tumor growth, suggesting that Mal2 is a potential target for breast cancer immunotherapy.
2020-01-23 | GSE144099 | GEO
Project description:Fibrinogen deposition promotes metastasis in lung because fibrinogen binds circulating tumor cells and the fibrinogen-tumor cell complex is allowed to invade in the lung tissue. We used microarrays to compare gene expression profiles of the tissues near and apart from fibrinogen deposition in non-cancer patients and cancer patients.
2023-05-26 | GSE211528 | GEO
Project description:Ligation of the B cell antigen receptor (BCR) initiates humoral immunity. However, mere BCR signaling without appropriate co-stimulation commits B cells to death rather than to differentiation into immune effector cells. How BCR activation depletes potentially autoreactive B cells while simultaneously primes for receiving rescue and differentiation signals from cognate T lymphocytes remains unknown. Here, using a mass spectrometry-based proteomic approach to identify cytosolic/nuclear shuttling elements, we uncover transcription factor EB (TFEB) as a central BCR-controlled rheostat that drives activation-induced apoptosis, and concurrently, promotes the reception of co-stimulatory rescue signals by supporting B cell migration and antigen presentation. CD40 co-stimulation prevents TFEB-driven cell death, while enhancing and prolonging TFEB’s nuclear residency, which hallmarks antigenic experience also of memory B cells. In mice, TFEB shapes the transcriptional landscape of germinal center B cells. Within the germinal center, TFEB facilitates the dark zone entry of light-zone-residing centrocytes through regulation of chemokine receptors and, by balancing the expression of Bcl-2/BH3-only family members, integrates antigen-induced apoptosis with T cell-provided CD40 survival signals. Thus, TFEB reprograms antigen-primed germinal center B cells for cell fate decisions.
2024-08-08 | PXD054505 | Pride