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In vitro activation of Btnl-1 transduced MODE-K cells with different stimuli

ABSTRACT: The experiment was designed to assess how intestinal epithelial cells respond to different soluble factors produced by intraepithelial lymphocytes (IEL) and how this response is altered when the epithelial cells express Btnl1.

ORGANISM(S): Mus musculus

PROVIDER: GSE63364 | GEO | 2015/03/31

SECONDARY ACCESSION(S): PRJNA267565

REPOSITORIES: GEO

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In vitro activation of Btnl-1 transduced MODE-K cells with different stimuli

Project description:The experiment was designed to assess how intestinal epithelial cells respond to different soluble factors produced by intraepithelial lymphocytes (IEL) and how this response is altered when the epithelial cells express Btnl1. Total RNA of MODE-K cells transduced with Btnl1-GFP or GFP alone and stimulated with TNF+IL-1_ in comparison to medium and with supernatant from anti-CD3-activated IEL in comparison to supernatant from unstimulated IEL

2015-03-31 | E-GEOD-63364 | biostudies-arrayexpress

Comprehensive proteomics analyses of IL-15 driven activation of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial lymphocytes (IEL) are an abundant population of tissue-resident T cells that protect the gut from pathogens and maintain intestinal homeostasis. The cytokine IL-15 is trans-presented by epithelial cells to IEL in complex with the IL-15 receptor α chain (IL-15Rα) and plays essential roles both in maintaining IEL homeostasis, and in inducing IEL activation in response to epithelial stress. When overproduced, IL-15 is a key driver of the gluten-induced enteropathy Coeliac disease, through cytotoxic activation of IEL. To better understand how IL-15 directly regulates both homeostatic and inflammatory functions of IEL, we performed quantitative proteomics of IL-15/Rα-stimulated murine IEL, sorted into their 3 main subpopulations, TCRγδ CD8αα, TCRαβ CD8αβ and TCRαβ CD8αα expressing IEL. The data reveal that high IL-15/Rα stimulation licenses cell cycle activation, upregulates the biosynthetic machinery in IEL, increases mitochondrial respiratory capacity and induces expression of cell surface immune receptors and adhesion proteins that potentially drive IEL activation.

2021-05-10 | PXD025891 | Pride

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Expression data from mouse small intestinal γδ intraepithelial lymphocytes

Project description:The mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined. In this study, we used microarrays to uncover the transcriptional responses that occur in small intestinal γδ intraepithelial lymphocytes following bacterial challenge. γδ intraepithelial lymphocytes (γδ IEL) were isolated by flow cytometry from the small intestines of germ-free mice, or from age- and sex-matched conventionally-raised counterparts. We extracted RNAs from these purified γδ IEL for analysis on Affymetrix DNA microarrays. The mice were all >8 weeks in age, and each sample represents a pool of RNAs from 5-8 mice.

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Project description:We report the application of RNA-Seq technology for high-throughput gene expression profiling of intestinal intraepithelial lymphocytes (IEL) that were incubated for 24 hrs in the presence or absence of recombinant osteopontin.

2018-11-01 | GSE122007 | GEO

Mus musculus

Project description:Anti-CD3-induced activation of intestinal intraepithelial lymphocytes (IEL)

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Gene expression of conventional and unconventional T cell subsets

Project description:The experiments were designed to gain insight into the gene expression of conventional and unconventional murine T cell subsets in the steady state and upon activation TCRαβ and TCRγδ intraepithelial lymphocytes (IEL) isolated from murine gut, naïve and virus-induced memory splenocytes, activated dendritic epidermal T cells (DETC)

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Project description:Intraepithelial lymphocytes (IELs) reside in the epithelial layer to protect against foreign pathogens and maintain epithelial barrier functions in the intestine. The interaction between IELs and epithelial cells is required for their functions; however, the underlying molecular machinery still remains to be elucidated. Here, we found that intestinal epithelium-specific deficiency in a clathrin adaptor protein (AP)-1B, which regulates the basolateral protein sorting, led to the massive reduction of IELs. Quantitative proteomics demonstrated that dozens of proteins, including known IEL-interacting proteins—E-cadherin, Btnl2, and Plexin B2—decreased in the basolateral membrane of AP-1B-deficient epithelial cells. Among the downregulated proteins, CD166 is included. CD166 interacted with CD6 on the surface of induced IELs. CD166 knockdown using shRNA in intestinal organoid culture significantly inhibited the recruitment of IELs to an epithelial layer. These data suggest that basolateral sorting by AP-1B is indispensable for maintaining IELs in the epithelial layer and survival of IELs.

2024-09-26 | PXD042900 | JPOST Repository

Transcription profiling of mouse small intestine intraepithelial lymphocytes (IEL) vs. TCR ab+ CD8b+ and TCR gd+ cells

Project description:Mouse small intestine intraepithelial lymphocytes (IEL) that express a ab TCR and CD8aa homodimers are an enigmatic T cell subset, as their specificity and in vivo function remain to be defined. To gain insight into the nature of these cells, we performed global gene expression profiling using microarray analysis, combined with PCR and flow cytometry to determine the level of expression of selected genes. Using these methods, TCR ab+ CD8aa IEL were compared to their TCR ab+ CD8b+ and TCR gd+ counterparts. Experiment Overall Design: In this study, the three IEL populations were isolated by cell sorting from a pool of IELs from 20 mice. RNA from each IEL subset was used to probe one microarray. A replicate experiment was performed on a seperate occasion using a new pool of 20 mice and three additional microarrays were used.

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