Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA130469 | ENA |
REPOSITORIES: ENA
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Project description:Human retinal pigment epithelial (HRPE) cells in culture respond to inflammatory cytokines (IFN-γ + TNF-α + IL-1β ) by increasing the expression of many cytokines and chemokines. The goal of this study was to delineate the role of miRNA in this process. We employed microarray analysis to study the effect of inflammatory cytokines on the miRNA expression in HRPE cells.
2010-11-11 | GSE23979 | GEO
Project description:A protein microarray kit (QAR-INF-1-2, RayBiotech Life Inc., Norcross, GA, USA) was used to detect 10 kinds of inflammatory factors in the CSF and serum (nN=5 per group), including IFN-γ, IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-13, MCP-1, and TNF-α.
2023-04-03 | GSE228521 | GEO
Project description:Analysis of MIN6 murine beta cell line transfected with ARH3 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.
2024-05-21 | PXD021501 | Pride
Project description:Analysis of MIN6 murine beta cell line transfected with Pla2g6 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.
2024-02-08 | PXD017863 | Pride
Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).
2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress
Project description:We report the transcriptome of human endothelial cells (cell line: TIME) after supplementation with polyunsaturated fatty acids (PUFA) and/or stimulation with pro-inflammatory cytokines. The fatty acids docosahexaenoic acid (DHA, C22:6n3) or arachidonic acid (AA, C20:4n6) were included in the culture medium in concentrations of 15 µmol/L using ethanol as a vehicle (0.2 % v/v final ethanol concentration). Cells were cultured in the enriched media totaling 144 h. Stimulation of cells was performed in the last 24 h of fatty acid supplementation by addition of the cytokines IL-1β, TNF-α, and IFN-γ each in a concentration of 5 ng/ml.
2021-12-01 | GSE141957 | GEO
Project description:Aims/Hypothesis: Type 1 diabetes (T1D) is an autoimmune disease marked by the destruction of beta cells in the pancreatic islets, with an incomplete picture of disease pathogenesis/progression and a lack of definitive cure. A recent finding linked pancreatic ductal cells of T1D donors with elevated levels of human leukocyte antigen (HLA) Class II molecules; however, the causal relationship and functional significance of this finding remain unknown. Because HLA Class II molecules are typically expressed by professional antigen presenting cells (APCs), this raises the possibility of ductal cells functioning as non-professional APCs. In this study, we test the hypothesis that non-T1D ductal cells are responsive to T1D-associated proinflammatory cytokines, TNF-α, IL-1β, and IFN-γ, and can act as non-professional APCs. Methods: Pancreatic exocrine cells, after the removal of islets, were obtained from cadaveric donors without apparent diseases and with appropriate consent. Cells were cryopreserved, thawed into a defined culture medium tailored to support ductal cell survival in a 3D suspension culture system. Ductal cells were exposed to various doses of cytokines for 48 hours and analyzed for gene and protein expression, using qRT-PCR, bulk-RNAseq, flow cytometry and Western blot analyses. Functional ability of cytokine-treated ductal cells to present an exogenous autoantigen (glutamate decarboxylase 65kD isoform [GAD65]) to T cells was tested using a GAD65-specific autoreactive CD4+ T cell clone (named BRI4.13) isolated from a T1D donor. Results: We found that within 48 hours a combination of TNF-α, IL-1β, and IFN-γ stimulated the expression of HLA Class II, co-stimulatory, and antigen-processing molecules at mRNA and protein levels in non-T1D ductal cells. Bulk RNAseq analysis showed that cytokines most significantly upregulated biological pathways in “antigen processing and presentation” and “T1D”. When cytokine-treated ductal cells were pulsed with an exogenous GAD65 peptide and cocultured with the BRI4.13 T cells, these T cells became activated and proliferated. Unexpectedly, we also found ~1% of KRT19+ ductal cells express GAD protein endogenously. Conclusions/interpretation: These results demonstrate that non-diseased primary ductal cells are sensitive to TNF-α, IL-1β, and IFN-γ stimulation, and can upregulate APC molecules and function in antigen presentation to autoreactive CD4+ T cells. To the best of our knowledge, our results provide the first evidence demonstrating antigen presentation by non-T1D human ductal cells to T cells, which implicate ductal cells in contributing to T1D progression.
2025-09-30 | GSE309294 | GEO
Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. Human islets were isolated and exposed (or not) to IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix arrays. These measurements were performed three times.
2013-12-19 | E-GEOD-53454 | biostudies-arrayexpress
Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. INS1 cell lines were cultured in medium with or without IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix Rat ST arrays. These experiments were performed on two separate occasions.
2013-12-19 | E-GEOD-53453 | biostudies-arrayexpress
Project description:Transcriptional response of KBM7 cells to IFN-gamma or TNF-alpha was investigated in control or cells with genetrap insertions in JAK2 or TNFRS1A, respectively. The experiment shows that, as expected, cells lacking JAK2 or TNFRS1A expression display a severly blunted response to the tested cytokines. KBM7 genetrap mutant cells stimulated with TNF-alpha and IFN-gamma Sample WT_1 corresponds with the control sample for the IFN-gamma stimulation; Sample WT_2 corresponds with the control sample for the TNF-alpha stimulation. As the expected differences between the samples was large, only single replicates were performed for each condition
2013-08-09 | E-GEOD-48848 | biostudies-arrayexpress