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Cell specific response to IFNg

ABSTRACT: Cell specific response to IFNg

OTHER RELATED OMICS DATASETS IN: GSE112876

PROVIDER: PRJNA449370 | ENA |

REPOSITORIES: ENA

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Cell specific response to IFNg

Project description:We report cell specific responses to IFNg in 11 different peripheral immunocyte populations in the mouse. These cells represent the core ImmGen immunocyte lineage panel. Profiles from these were used to analyze cell specific responses to IFNg. In general a core set of ISG transcripts are induced in all cells. Smaller sets of ISGs were induced in a cell specific manner. In particular, splenic granulocytes and dendritic cells show restriced indcution of sets of ISGs.

2018-04-10 | GSE112876 | GEO

Peritoneal cavity macrophage response to IFNg and IFNa

Project description:We seeked to determine in vivo effects of IFNg and IFNa response in peritoneal cavity macrophages. These cells were part of ImmGen Interferon cytokine study and immunocytes were sorted according to Immgen's standard lineage panel. Profiles from peritoneal cavity macrophages were used to analyze cell specific responses to IFNg.

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NGS5522 - hMDMS response to IFNg and TNFa

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Project description:We did transcriptome profiling for monocytes treated with or without IFNg to characterize IFNg response.

2016-09-12 | GSE84691 | GEO

Peritoneal cavity macrophage response to IFNg and IFNa

Project description:Peritoneal cavity macrophage response to IFNg and IFNa

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IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood Ex vivo sorted Tregs (CD25highCD127neg) were stimulated for 4 hours and IFNg-secreting cells were detected by a IFNg-capture kit. The samples were resorted based on IFNg expression.

2016-07-01 | E-GEOD-71274 | biostudies-arrayexpress

NGS5522 - hMDMS response to IFNg and TNFa

Project description:human primay macrophages (hMDMs) were unstimulated, stimulated with IFNg or costimulated with IFNg and TNFa for 18h

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IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood

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GSK3a/b restrains IFNg-inducible costimulatory molecule expression in alveolar macrophages, limiting CD4+ T cell activation

Project description:Macrophages play a crucial role in eliminating respiratory pathogens. Both pulmonary resident alveolar macrophages (AMs) and recruited macrophages contribute to detecting, responding to, and resolving infections in the lungs. Despite their distinct functions, it remains unclear how these macrophage subsets regulate their responses to infection, including how activation by the cytokine IFNg is regulated. This shortcoming prevents the development of therapeutics that effectively target distinct lung macrophage populations without exacerbating inflammation. We aimed to better understand the transcriptional regulation of resting and IFNg-activated cells using a new ex vivo model of AMs from mice, fetal liver-derived alveolar-like macrophages (FLAMs), and immortalized bone marrow-derived macrophages (iBMDMs). Our findings reveal that IFNg robustly activates both macrophage types; however, the profile of activated IFNg-stimulated genes varies greatly between these cell types. Notably, FLAMs show limited expression of costimulatory markers essential for T cell activation upon stimulation with only IFNg. To understand cell type-specific differences, we examined how the inhibition of the regulatory kinases GSK3a/b alters the IFNg response. GSK3a/b controlled distinct IFNg responses, and in AM-like cells, we found GSK3a/b restrained the induction of type I IFN and TNF, thus preventing the robust expression of costimulatory molecules and limiting CD4+ T cell activation. Together, these data suggest that the capacity of AMs to respond to IFNg is restricted in a GSK3a/b-dependent manner and that IFNg responses differ across distinct macrophage populations. These findings lay the groundwork to identify new therapeutic targets that activate protective pulmonary responses during infection without driving deleterious inflammation.

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