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TranscriptomicsIL-10 from intestinal macrophages prevents excessive innate immune responses to bacteria by limiting IL-23 synthesis
Innate immune responses must be regulated in the intestine to prevent excessive inflammation. Here, using gene reporter mice, we show that a subset of mouse colonic macrophages constitutively produced the anti-inflammatory cytokine IL-10. In mice infected with Citrobacter rodentium, which is consid...
ORGANISM(S): Mus musculus 
2015-05-12 | E-GEOD-58677 | biostudies-arrayexpress
ProteomicsMouse Th17 T cells, IL-23 stimulated
Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to character...
ORGANISM(S): Mus musculus (Mouse) 
2020-03-25 | PXD016633 | Pride
Th17 Mouse T lymphocyte Il-23 
TranscriptomicsSuppression of molecular inflammatory pathways by Toll-like Receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation
Psoriasis is a complex inflammatory disease resulting from the activation of T helper (Th) 1 and Th17 cells. Recent evidence suggests that abnormal activation of Toll-like receptors (TLRs) 7, 8 and 9 contributes to the initiation and maintenance of psoriasis. We have evaluated the effects of TLR a...
ORGANISM(S): Mus musculus 
2014-01-21 | E-GEOD-50400 | biostudies-arrayexpress
ModelsImmunological Model of sphingolipids with IL-6/IL-17/IL-23 in L. major infection
In diseased state, we demonstrated that increase in production of sphingosine-1-phosphate and overexpression of IL-6,lL-17 and IL-23 with SATB1 leads to disease progression.
2023-01-11 | MODEL2301110001 | BioModels
ModelsImmunological Healthy State Model of Sphingolipids with IL-6/IL-17/IL-23 immune axis in L.major infection
In Healthy State, we demonstrated the controlled expression of sphingolipids and the controlled IL-6,IL-17,IL-23 cytokines signalling via SOCS3 mediated regulation.
2023-01-11 | MODEL2301110002 | BioModels
GenomicsInterleukin-23-induced transcription factor Blimp1 promotes pathogenicity of T helper 17 cells
Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory fun...
ORGANISM(S): Mus musculus 
2016-06-15 | E-GEOD-75724 | biostudies-arrayexpress
TranscriptomicsNFAT-dependent IL-2 and IL-23 produced by DC are key regulators of pathogenic (TH17-mediated lung inflammation)
Calcineurin/NFAT/IL-2 signaling pathway is activated in dendritic cells (DC) upon encounter of β glucan, the main component of the fungal cell wall, raising the question about the role of NFAT-regulated genes in DC biology in vivo. To directly assess the function of IL-2 secreted by DC, we analyzed...
ORGANISM(S): Mus musculus 
2015-12-21 | E-GEOD-58590 | biostudies-arrayexpress
TranscriptomicsInduction and molecular signature of pathogenic Th17 cells
TGF-beta3 produced by developing Th17 cells induces highly pathogenic T cells that are functionally and molecularly distinct from TGF-beta1-induced Th17 cells. The microarray data represent a distinct molecular signature for pathogenic versus non-pathogenic Th17 cells. Total of seven groups with two...
ORGANISM(S): Mus musculus 
2012-09-01 | E-GEOD-39820 | biostudies-arrayexpress
GenomicsEnhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-β Signaling: ChIPSeq
CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity. Crucial for T helper17 (Th17) cells in vivo, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to ...
ORGANISM(S): Mus musculus 
2010-08-31 | E-GEOD-23681 | biostudies-arrayexpress
GenomicsHigh-resolution, patient-level dissection of IL-23 blockade in cutaneous psoriasis
Psoriasis vulgaris and other chronic inflammatory diseases improve markedly with therapeutic blockade of IL-23 signaling in T cells, but the genetic mechanisms of response remain poorly understood. We single-cell transcriptomically profiled CD45+ immune cells isolated from lesional psoriatic skin be...
EGAS00001007373 | EGA
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