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Murine gamma delta intraepithelial lymphocyte response to type I IFN and TCR blockade

ABSTRACT: Murine gamma delta intraepithelial lymphocyte response to type I IFN and TCR blockade

PROVIDER: PRJNA1090425 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28408760_1.fastq.gz	Fastqsanger.gz
	SRR28408760_2.fastq.gz	Fastqsanger.gz
	SRR28408761_1.fastq.gz	Fastqsanger.gz
	SRR28408761_2.fastq.gz	Fastqsanger.gz
	SRR28408762_1.fastq.gz	Fastqsanger.gz

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Murine gamma delta intraepithelial lymphocyte response to type I IFN and TCR blockade

Project description:Interferon alpha (IFNa) is a pro-inflammatory cytokine that is rapidly upregulated as part of an innate immune response. Gamma delta intraepithelial lymphocytes (gd IEL) mount a rapid antimicrobial response to luminal microorganisms and previous report indicate that the T cell receptor (TCR) of these cells is constantly triggered at steady-state. We assessed the contribution of tonic TCR activation in response to acute, systemic IFNa administration among murine gd IELs. Our data demonstrate that inhibiting basal TCR signaling has a minimal effect on the transcriptional profile of gd IELs and acute IFNa exposure induces antiviral gene programs independent of TCR signaling.

2024-10-01 | GSE262121 | GEO

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

Comparison of gamma delta intraepithelial lymphocytes from DSS-treated and untreated colon

Project description:gamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray. Duplicate comparisons were made between DSS-treated and untreated gamma delta intraepithelial lymphocytes.

2008-12-18 | E-GEOD-13946 | biostudies-arrayexpress

Microbiota promote enhanced CD39 expression in gamma delta (gd) intraepithelial lymphocytes through the activation of TCR and IL-15 signaling.

Project description:Intraepithelial lymphocytes expressing the gd T cell receptor (gd IEL) provide continuous surveillance of the intestinal epithelium. We report that mice harboring a microbiota-specific hyperproliferative gd IEL (gdHYP) phenotype also upregulate the expression of the ectonucleotidase CD39, a marker of regulatory gd T cells. Enhanced TCR and IL-15 signaling correlates with a progression from a naïve-like CD39neg gd IEL to a more mature, tissue-adapted CD39hi IEL population. We find that TCRgd activation drives CD122-mediated CD39 upregulation on gdHYP IELs and increased mucosal IL-15 further amplifies CD39 expression in gdHYP IELs. Notably, CD39 induction requires sustained exposure to the gdHYP-associated microbiota. Increased IL-15 signaling prolongs IEL survival and enhances gdHYP IEL bioenergetic potential. Notably, CD39hi gd IELs produce less pro-inflammatory cytokine, which may explain the lack of histopathology in gdHYP mice. Overall, our study identifies a previously unappreciated mechanism by which an altered microbiota amplifies CD39 expression on gdHYP IELs, leading to the expansion of gd IELs with regulatory potential.

2025-08-27 | GSE292555 | GEO

Stepwise chromatin and transcriptional acquisition of an intraepithelial lymphocyte program

Project description:Mesenteric lymph node (mLN) T cells undergo tissue adaptation upon migrating to intestinal lamina propria (LP) and intraepithelial (IE) compartments, ensuring appropriate balance between tolerance and resistance. By combining mouse genetics with single-cell and chromatin analyses, we addressed the molecular imprinting of gut epithelium on T cells. Transcriptionally, conventional and regulatory (Treg) CD4+ T cells from mLN, LP and IE segregate based on the gut layer they occupy; trajectory analysis suggests a stepwise loss of CD4-programming and acquisition of an intraepithelial profile. Treg fate–mapping coupled with RNA– and ATAC–sequencing revealed that the Treg program shuts down before an intraepithelial program becomes fully accessible at the epithelium. Ablation of CD4 lineage–defining transcription factor ThPOK results in premature acquisition of an IEL profile by mLN Tregs, partially recapitulating epithelium imprinting. Thus, coordinated replacement of circulating lymphocyte program with site–specific transcriptional and chromatin changes is necessary for tissue imprinting.

2021-01-04 | GSE146292 | GEO

Identification of Ligands for the human gamma-delta TCR

Project description:T cells bearing gamma delta T cell antigen receptors (TCRs) function in lymphoid stress surveillance. However, the contribution of gamma delta TCRs to such responses is unclear. Here we found that the TCR of a human V gamma4Vdelta5 clone directly bound endothelial protein C receptor (EPCR), which allowed gamma delta T cells to recognize both endothelial cells targeted by cytomegalovirus and epithelial tumors. EPCR is a major histocompatibility complex–like molecule that binds lipids analogously to the antigen-presenting molecule CD1d. However, the V gamma4Vdelta5 TCR bound EPCR independently of lipids, in an antibody-like way. Moreover, the recognition of target cells by gamma delta T cells required a multimolecular stress signature composed of EPCR and costimulatory ligand(s). Our results demonstrate how a gamma delta TCR mediates recognition of broadly stressed human cells by engaging a stress-regulated self antigen. 2E9 is an antibody that blocks gd-TCR recognition of human cells that are the targets of the clone LES. 2E9 also stains cells that are targeted by LES. Therefore, to identify the TCR ligand expressed by 2E9-positive cells, Gene Expression was compared in two cell lines that stain with 2E9 (K562 and U937) versus two cell lines that do not (Hutu80 and Huh7).

2012-07-27 | E-GEOD-39709 | biostudies-arrayexpress

Comparison of gamma delta intraepithelial lymphocytes from DSS-treated and untreated colon

Project description:gamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray.

2008-12-18 | GSE13946 | GEO

Stepwise chromatin and transcriptional acquisition of an intraepithelial lymphocyte program

Project description:Stepwise chromatin and transcriptional acquisition of an intraepithelial lymphocyte program

| PRJNA610060 | ENA

Identification of Ligands for the human gamma-delta TCR

2012-07-28 | GSE39709 | GEO

Newly recruited intraepithelial Ly6A+CCR9+CD4+ T cells protect against enteric viral infection

Project description:The intestinal epithelium comprises the body’s largest surface exposed to viruses. Additionally, the gut epithelium hosts a large population of intraepithelial T lymphocytes, or IELs, although their role in resistance against viral infections remain elusive. By fate-mapping T cells recruited to the murine intestine, we observed accumulation of newly recruited CD4+ T cells after infection with murine norovirus CR6 and adenovirus type-2 (AdV), but not reovirus. CR6 and AdV-recruited intraepithelial CD4+ T cells co-express Ly6A and CCR9, exhibit T helper 1 and cytotoxic profiles and confer protection against AdV in vivo and in an organoid model in an IFN-g-dependent manner. Ablation of the T cell receptor (TCR) or the transcription factor ThPOK in CD4+ T cells prior to AdV infection prevented viral control, while TCR ablation during infection did not impact viral clearance. These results uncover a protective role for intraepithelial Ly6A+CCR9+CD4+ T cells against enteric adenovirus.

2022-05-26 | GSE196417 | GEO

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