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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human primary keratinocytes treated with either IL-17, IL-22 or IFNg

ABSTRACT: In this study, we shought to identify the cytokines produced by skin-resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors. Experiment Overall Design: In this study, primary keratinocytes were treated with either IL-17, IL-22 or IFNg for 24 hours then harvested for RNA extraction and subsequent gene array analysis

ORGANISM(S): Homo sapiens

SUBMITTER: Mayte Suarez-Farinas

PROVIDER: E-GEOD-12109 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways

Project description:In this study, we shought to identify the cytokines produced by skin-resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors. Keywords: repeated measures experiment

2008-07-15 | GSE12109 | GEO

RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

Project description:The intestinal epithelium is our first line of defense against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. The changes in cellular composition is driven by immune cell derived cytokines. Here we use signature cytokines of different type of immune responses applied to small intestinal organoids to model how different immune responses affect intestinal epithelial development. Simplified, IFNG represents type I immunity against intracellular pathogens such as viruses, IL-13 represents type II immunity against infections such as parasites and IL-22 represents type III immunity against extracellular bacterial infections. To not influence organoid formation, organoids were grown 24 hours without cytokines, and then 10 ng/mL of cytokine was applied for 24 hours before harvesting RNA. Furthermore, IFNG is supplied in combination with the other cytokines as cytokines are rarely found alone in an inflammation setting. We find that these cytokines affect developmental pathways of the intestinal epithelium and affect the cellular composition of the intestinal epithelium.

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Primary Human Bronchial Epithelial Cells (HBEs) Stimulated with IL-22 and IL-17

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Transcription profiling of primary human bronchial epithelial cells stimulated with IL-22 and IL-17

Project description:Primary HBE cells were stimulated with IL-22 and IL-17, and gene expression was studied using an Affymetrix platform microarray, in order to investigate which genes may be upregulated or downregulated in response to these cytokines. Of particular interest was the host defense genes such as antimicrobial peptides, which have been shown to be upregulated by IL-22 and IL-17 in skin keratinocytes. Experiment Overall Design: There were 4 conditions to this study (media, IL-22, IL-17 and IL-22+17) and there were 3 biological replicates of each condition. Experiment Overall Design: Gene expression study using one timepoint of 24 hours after stimulating these primary cells with the above conditions

2008-06-11 | E-GEOD-10240 | biostudies-arrayexpress

Multiple IL-17 family cytokines signaling through IL-17RA drive inflammatory pathways in psoriasis

Project description:The IL-23/IL-17 immune axis is of central importance in psoriasis. However, the contribution of IL-17 family cytokines other than IL-17A to drive skin inflammation in psoriasis has not been fully established. To further elucidate the role of individual IL-17 family cytokines in psoriasis, we investigated their expression and localization in psoriasis skin at the mRNA and protein level. Moreover, we investigated the gene expression signatures induced by individual IL-17 family cytokines in human skin ex vivo as well as modulation of responses induced by the combination of IL-17 family cytokines in human keratinocytes by brodalumab, a human monoclonal antibody targeting the IL-17RA, versus the IL-17A blocking antibody ixekizumab. We demonstrate that IL-17A, IL-17AF, IL-17F and IL-17C are expressed at increased levels in psoriasis lesional skin and induce inflammatory gene expression signatures in human skin ex vivo that correlate with those observed in psoriasis. Furthermore, we show that brodalumab, in contrast to ixekizumab, fully blocks gene expression responses induced by the combination of IL-17A, IL-17AF, IL-17F and IL-17C in human keratinocytes. These findings suggest that inhibition of several IL-17 family cytokines, e.g. by targeting of the IL-17RA receptor, could be a favored mechanism to obtain a profound suppression of the inflammatory processes in psoriasis and thereby achieve high levels of skin clearance and sustained efficacy in patients with psoriasis.

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Gene expression profile of human epidermal keratinocytes in response to IFNgamma, IL-4, IL-6, IL-17A and IL-22

Project description:To understand the role of epidermal keratinocytes in immunopathology of skin diseases with predominant T helper (Th) cell responses, we measured the genome-wide transcriptional profile of human keratinocytes in response to IFNgamma, IL-4, IL-17A or IL-22, major cytokines produced by Th1, Th2, Th17 or Th22 cells, respectively. IL-6 was also included in the transcriptional profile analysis because a variety of pro-inflammatory stimuli stimulate human keratinocytes to produce IL-6 that has an autocrine or paracrine role in epidermal immunity. We aimed to discover commonly expressed genes in human keratinocytes in response to pro-inflammatory cytokines, which would be associated with common pathophysiological responses in various skin diseases such as skin permeability barrier disruption or epidermal hyperplasia. Normal human keratinocytes (NHKs) were stimulated with IFNγ, IL-4, IL-6, IL-17A and IL-22 for 24 hours and harvested for total RNA extraction and hybridization on Affymetrix microarrays.

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Human Treg IFNg/IL-10 subpopulations

Project description:Human Treg IFNg/IL-10 subpopulations

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IL-17 induces an expanded range of downstream genes in reconstituted human epidermis model

Project description:Background: IL-17 is the defining cytokine of the Th17, Tc17, and γδ T cell populations that plays a critical role in mediating inflammation and autoimmunity. Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines with relevant contributions of IFN-γ, TNF-α, and IL-17. Despite the pivotal role IL-17 plays in psoriasis, and in contrast to the other key mediators involved in the psoriasis cytokine cascade that are capable of inducing broad effects on keratinocytes, IL-17 was demonstrated to regulate the expression of a limited number of genes in monolayer keratinocytes cultured in vitro. Methodology/Principal Findings: Given the clinical efficacy of anti-IL-17 agents is associated with an impressive reduction in a large set of inflammatory genes, we sought a full-thickness skin model that more closely resemble in vivo epidermal architecture. Using a reconstructed human epidermis (RHE), IL-17 was able to upregulate 419 gene probes and downregulate 216 gene probes. As possible explanation for the increased gene induction in the RHE model is that CEBPβ, the transcription factor regulating IL-17-responsive genes, is expressed in differentiated KCs. Conclusions/Significance: The genes identified in IL-17-treated RHE are likely relevant to the IL-17 effects in psoriasis, since ixekizumab (anti-IL-17A agent) strongly suppressed the “RHE” genes in psoriasis patients treated in vivo with this IL-17 antagonist. RHE samples were treated with IFNg, IL-22 and IL-17 and compared with control

2014-02-28 | E-GEOD-52361 | biostudies-arrayexpress

Transcription profiling of human epidermal keratinocytes treated with IL-1

Project description:Interleukin-1 is a proinflammatory and immunomodulatory cytokine that plays a crucial role in inflammatory diseases of the skin, including bacterial infections, bullous diseases, UV damage and especially psoriasis. To characterize the molecular effects of IL-1 in epidermis, we defined the transcriptional changes in human epidermal keratinocytes 1, 4, 24, and 48 h after treatment with IL-1a. IL-1 significantly regulated 388 genes, including genes associated with proteolysis, adhesion, signal transduction, proliferation, and epidermal differentiation. IL-1 induces many genes that have antimicrobial function. Secreted cytokines, chemokines, growth factors, and their receptors are the prominent targets of IL-1 regulation, including IL-8, IL-19, elafin, C3, and S100A proteins, which implicates IL-1 in the pathogenesis of inflammatory diseases. IL-1 induced not only proliferation-associated genes but also differentiation marker genes such as transglutaminase-1 and involucrin, which suggests that IL-1 plays an important role in the aberrant proliferation and differentiation seen in psoriasis. Correlation of IL-1 regulated genes with the TNFa and IFNg regulated ones showed more similarities between IL-1 and TNFa than IL-1 and IFNg, whereas Oncostatin-M affected a largely unrelated set of genes. IL-1 regulates many genes previously shown to be specifically over-expressed in psoriasis. In summary, IL-1 regulates a characteristic set of genes that define its specific contribution to inflammation and aberrant differentiation in skin diseases. Experiment Overall Design: keratinocytes were treated with 25 ng/ml IL-1 and transcriptomes compared to untreated controls at 1, 4, 24 and 48 h post treatment.

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RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

Project description:RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

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