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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

Tissue adaptation is the dominant driver of the proteomic landscape of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial T lymphocytes (T-IEL) patrol the single layer of epithelial cells lining the gut, and consist of both induced T-IEL, derived from systemic antigen-experienced lymphocytes, and natural IEL, that are developmentally targeted to the intestine. To gain functional insights into these enigmatic cells, we used high-resolution quantitative mass spectrometry to investigate the proteomic landscape of the main T-IEL populations in the gut. Comparing the proteomes of induced T-IEL, tissue-resident memory TCRαβ+ CD8αβ+ cells and natural TCRγδ+ CD8αα+ and TCRαβ+ CD8αα+ T-IEL, with naive CD8+ T cells from lymph nodes reveals striking similarities between T-IEL subsets and the dominant effect of the gut environment on T-IEL phenotypes. Analysis of copy numbers/cell of >7000 proteins provides new understanding of the differences in composition of T cell antigen receptor signal transduction pathways in T-IEL versus conventional T cells and reveals skewing of the metabolic machinery towards an exhausted T cell phenotype adapted to the intestinal environment. This study provides a resource for exploring and understanding how multiple inputs are integrated into T-IEL function.

2021-03-15 | PXD023140 | Pride

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.

2011-04-06 | E-GEOD-28437 | biostudies-arrayexpress

The signaling pathway involved in wild type and 2D2-gut CD4+ T cell development

Project description:To find the signalling pathway involved in WT/2D2 CD4+ gut T cell (CD4+ intraepithelial lymphocytes, CD4+IEL) differentiation, particulary to determine whether aryl hydrocarbon receptor (AHR) pathway is involved.

2016-04-01 | GSE79748 | GEO

RNA Sequencing Gene Expression Profile of IEL Incubated In The Presence or Absence of Osteopontin

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

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)

2015-03-31 | E-GEOD-63090 | biostudies-arrayexpress

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.

2008-06-13 | E-GEOD-5355 | biostudies-arrayexpress

Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [scRNA-seq]

Project description:Intestinal intraepithelial lymphocytes (IEL) are capable of rapid innate-like responses to microenvironmental cues. While poised to activation, IEL effector functions must be stringently controlled. Aiolos is an Ikaros zinc finger (IKZF) family member encoded by Ikzf3 that promotes histone deacetylation. Here, we found that Aiolos is a crucial regulator of IEL activation. Ikzf3–/– CD8αα+ IEL expressed high levels of innate NK receptors, cytotoxic enzymes, cytokines and chemokines. Single cell RNAseq of IEL revealed that Ikzf3 deficiency mostly amplified the effector machinery of a CD8αα+ IEL subset characterized by high expression CD122, the receptor for IL-15. Furthermore, Ikzf3 deficiency increased IEL responsiveness to IL-15. Aiolos binding sites were close to those for STAT5 and RUNX transcription factors that promote IL-15 signaling and cytolytic programs, respectively; lack of Ikzf3 increased accessibility and histone acetylation of these chromatin regions. Ikzf3 deficiency increased susceptibility to colitis, demonstrating the functional relevance of Aiolos-mediated regulation of IEL effector functions.

2023-10-20 | GSE220028 | GEO

Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [CUT&RUN]

2023-10-20 | GSE220022 | GEO

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