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Nfkbid-overexpression and -ablation enhances thymic deletion of autoreactive AI4 CD8 T-cells

ABSTRACT: Nfkbid-overexpression and -ablation enhances thymic deletion of autoreactive AI4 CD8 T-cells

PROVIDER: PRJNA736716 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14779232.fastq.gz	Fastqsanger.gz
	SRR14779233.fastq.gz	Fastqsanger.gz
	SRR14779234.fastq.gz	Fastqsanger.gz
	SRR14779235.fastq.gz	Fastqsanger.gz
	SRR14779236.fastq.gz	Fastqsanger.gz

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Nfkbid-overexpression and -ablation enhances thymic deletion of autoreactive AI4 CD8 T-cells

Project description:Purpose: Analyze genes involved in the negative selection of CD4CD8 double positive thymocytes from NOD-AI4 control mice, NOD-AI4-Nfkbid-/- (KO) and NOD-AI4-60A undergoing negative selection. Methods: RNA-Seq based gene expression analyses were used to identify differentially expressed genes in CD4CD8 double positive thymocytes from NOD-AI4 (control), NOD-AI4-Nfkbid-/- (KO) and NOD-AI4-60A undergoing negative selection.

2022-05-16 | GSE176566 | GEO

Nfkbid represents an Idd7 locus gene contributing to impaired thymic deletion of CD8 T-cells in NOD mice

Project description:In both NOD mice and humans, the development of type 1 diabetes (T1D) is dependent in part on autoreactive CD8+ T-cells recognizing pancreatic ß-cell peptides presented by often quite common MHC class I variants. Studies in NOD mice previously revealed the common H2-Kd and/or H2-Db class I molecules expressed by this strain acquire an aberrant ability to mediate pathogenic CD8 T-cell responses through interactions with T1D susceptibility (Idd) genes outside the MHC. A gene(s) mapping to the Idd7 locus on proximal Chromosome 7 was previously shown to be an important contributor to the failure of the common class I molecules expressed by NOD mice to mediate the normal thymic negative selection of diabetogenic CD8+ T-cells. Using an inducible model of thymic negative selection and mRNA transcript analyses we initially identified an elevated Nfkbid expression variant as a strong candidate for an NOD Idd7 region gene contributing to impaired thymic deletion of diabetogenic CD8+ T-cells. CRISPR/Cas9-mediated genetic attenuation of Nfkbid expression in NOD mice resulted in improved negative selection of autoreactive diabetogenic AI4 and NY8.3 CD8+ T-cells. These results indicated allelic variants of Nfkbid represent an Idd7 gene contributing to the efficiency of intrathymic deletion of diabetogenic CD8+ T-cells. However, while enhancing thymic deletion of pathogenic CD8+ T-cells, ablation of Nfkbid expression surprisingly accelerated T1D onset in NOD mice likely by numerically decreasing regulatory T- and B-lymphocytes (Tregs/Bregs), thereby reducing their peripheral immunosuppressive effects. We used microarray analysis to identify differentialy expressed genes in thymus under conditions of induced thymic negative selection. We compare two mice strains, NOD-LCMV vs NOD.Ln82-LCMV (a congenic stock for a C57BL/6 derived segment delimited by markers D7Mit117–D7Mit247).

2018-06-14 | GSE115754 | GEO

Murine bone marrow immature B cells: autoreactive versus non-autoreactive

Project description:Transcriptional profiling of mouse bone marrow B220+CD23–CD43–IgD– autoreactive immature B cells from 3-83Igi,Rag1-/-,H-2b mice relative to non-autoreactive immature B cells from 3-83Igi,H-2d mice. Goal was to determine genes that potentially mediate negative and positive selection of immature B cells. Biological replicates: 2 autoreactive replicate against, 2 non-autoreactive replicates

2010-08-31 | E-GEOD-22802 | biostudies-arrayexpress

BCR repertoire analyis of class-switched and non-switched thymic B cells

Project description:We report that a large percentage of thymic B cells undergo class switching intrathymically. Thymic B cell class switching requires cognate T-B interaction. To determine whether B cell specificity was also important for thymic B cell class-switching, we sorted class-switched thymic B cells (CD19+B220+IgM-IgD-), unswitched B cells (CD19+B220+IgM+IgD+) and bulk splenic B cells in 3H9 heavy chain-fixed mice and performed high throughput sequencing analysis of the light chain of these populations. Results of this analysis indicated that class-switched thymic B cells have a distinct repertoire compared with unswitched thymic B cells and splenic B cells. Further reactivity tests indicated that a large part of BCRs enriched in class-switched thymic B cells are autoreactive. These data suggest that autoreactive B cells are selected into class-switched population and expanded in the thymus. Light chain repertoire profiles of class-switched thymic B cells, unswithced thymic B cells and splenic B cells from 3H9 mice were generated by deep sequencing.

2016-08-10 | E-GEOD-85366 | biostudies-arrayexpress

BCR repertoire analyis of class-switched and non-switched thymic B cells

2016-08-10 | GSE85366 | GEO

Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis

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Ablation of adipocyte BCL6 enhances subcutaneous adiposity and insulin sensitivity

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Thymic epithelial cells co-opt lineage-defining transcription factors to eliminate autoreactive T cells

Project description:Thymic epithelial cells co-opt lineage-defining transcription factors to eliminate autoreactive T cells

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Tissue restricted antigen expression by medullary thymic epithelial cell subsets induces distinct autoreactive T cell fates

Project description:Cellular interactions in the thymus play an essential role in ensuring the development of a self-tolerant T cell repertoire. Medullary thymic epithelial cells (mTECs) contribute to tolerance by expressing and presenting tissue-restricted antigens (TRA) so that developing T cells can assess the self-reactivity of their antigen receptors prior to leaving the thymus. This has largely been studied in the context of autoimmune regulator (Aire) dependent TRA expression in mature mTECs. Yet, mTECs are a heterogeneous population of cells that differentially express unique pools of TRA, and whether mTEC subsets induce distinct autoreactive T cell fates remains unclear. Here we attribute unique roles for mTEC subsets in directing distinct mechanisms of T cell tolerance that significantly impact infection and tumor control. These results have important implications in the design of effective therapeutic approaches that aim to modulate the function of self-reactive T cells.

2020-06-26 | GSE153288 | GEO

Bi-directional signaling by membrane-bound KitL induces proliferation and co-ordinates thymic endothelial cell and thymocyte expansion

Project description:The ligand for the c-Kit receptor, KitL, exists as a membrane-associated (mKitL) and a soluble form (sKitL). KitL functions outside c-Kit activation have not been identified. We show that co-culture of c-Kit– and mKitL–expressing NIH3T3 cells results in signaling through mKitL: c-Kit–bound mKitL recruits calcium-modulating cyclophilin ligand (CAML) to selectively activate Akt, leading to CREB phosphorylation, mTOR pathway activation, and increased cell proliferation. Activation of mKitL in thymic vascular endothelial cells (VECs) induces mKitL- and Akt-dependent proliferation, and genetic ablation of mKitL in thymic VECs blocks their c-Kit responsiveness and proliferation during neonatal thymic expansion. Therefore, mKitL–c-Kit form a bi-directional signaling complex that acts in the developing thymus to coordinate thymic VEC and early thymic progenitor (ETP) expansion by simultaneously promoting ETP survival and VEC proliferation. This mechanism may be relevant to both normal tissues and malignant tumors that depend on KitL–c-Kit signaling for their proliferation.

2018-11-21 | PXD011061 | Pride

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