Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB11897 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Medullary thymic epithelial cells (mTECs) play a critical role in central immune tolerance by mediating negative selection of autoreactive T cells through the collective expression of the peripheral self-antigen compartment, including tissue-specific antigens (TSAs). Recent work has shown that gene expression patterns within the mTEC compartment are remarkably heterogenous and include multiple differentiated cell states. To further define mTEC development and medullary epithelial lineage relationships, we combined lineage tracing and recovery from transient in vivo mTEC ablation with single cell RNA-sequencing in Mus musculus. The combination of bioinformatic and experimental approaches revealed a non-stem transit-amplifying population of cycling mTECs that preceded Aire expression. Based on our findings, we propose a branching model of mTEC development wherein a heterogeneous pool of transit-amplifying cells gives rise to Aire- and Ccl21a-expressing mTEC subsets. We further use experimental techniques to show that within the Aire-expressing developmental branch, TSA expression peaked as Aire expression decreased, implying Aire expression must be established before TSA expression can occur. Collectively, these data provide a higher order roadmap of mTEC development and demonstrate the power of combinatorial approaches leveraging both in vivo models and high-dimensional datasets.
2020-11-24 | GSE137699 | GEO
Project description:Single cell analysis of transit-amplifying thymic epithelial cells
| PRJDB11896 | ENA
Project description:RNA-seq analysis of transit-amplifying Aire+ mTECs
| PRJDB9868 | ENA
Project description:Comparative gene expression profiling analysis of RNA-seq data from CD49f+NGFR+, CD49f-NGFR- cell sorted from differentiated MTEC cultures collected at ALI day 10, and MTEC culture taken at ALI t0
2023-01-31 | GSE209678 | GEO
Project description:Antigen presentation by cortical and medullary thymic epithelial cells (cTEC and mTEC) ensures the formation of a self-restricted and self-tolerant T cell repertoire, respectively. As such, a broad diversity of self-antigens needs to be presented by mTEC to induce T cell’s self-tolerance. Even though the expression and antigen presentation of protein coding genes in mTEC has been abundantly described, little is known of the implication of allegedly noncoding regions of the genome to tolerance induction. In this study, we focused on transposable elements (TE), which have been shown to be highly expressed by mTEC.
2024-04-17 | PXD042241 | Pride
Project description:This study set out to assay the (polyA+) transcriptomes of single mature (MHCII high) mouse medullary thymic epithelial cells (mTEC). Following isolation by FACs, the transcriptomes of single mature mTEC was assayed using the Fluidigm C1 microfluidics platform and Illumina RNA-seq.
2014-09-04 | E-GEOD-60297 | biostudies-arrayexpress
Project description:Thymic medullary epithelial cell (mTEC) expression of the autoimmune regulator AIRE, and of tissue-specific antigens, is controlled by members of the non-canonical NF-kB signalling pathway, including RelB and NF-kB2. Of the genes in this pathway, RelB-/- mice develop a particularly severe multi-organ autoimmune syndrome, resembling Foxp3-deficiency. RelB-/- mice have medullary atrophy and few mTECs but the mechanism is unknown. We show that RelB is required for expression of medullary chemokines and mTEC AIRE, selection of a diverse peripheral T cell repertoire, and for peripheral Foxp3+ Treg function. Vβ families of T cells infiltrating diseased peripheral organs and thymic Treg were similarly skewed. Surprisingly, medullary atrophy results from intra-thymic granulocyte infiltration, consequent upon the Th2-mediated autoimmune disease. Dominant tolerance corrects thymic inflammatory disease and loss of thymic function. We demonstrate a reversible RelB-dependent inflammatory mechanism for loss of central tolerance associated with medullary atrophy. Thymi from 4 RelB+/- mice and 3 RelB-/- mice were profiled by microarays
2012-12-27 | E-GEOD-43154 | biostudies-arrayexpress
Project description:Thymic medullary epithelial cell (mTEC) expression of the autoimmune regulator AIRE, and of tissue-specific antigens, is controlled by members of the non-canonical NF-kB signalling pathway, including RelB and NF-kB2. Of the genes in this pathway, RelB-/- mice develop a particularly severe multi-organ autoimmune syndrome, resembling Foxp3-deficiency. RelB-/- mice have medullary atrophy and few mTECs but the mechanism is unknown. We show that RelB is required for expression of medullary chemokines and mTEC AIRE, selection of a diverse peripheral T cell repertoire, and for peripheral Foxp3+ Treg function. Vβ families of T cells infiltrating diseased peripheral organs and thymic Treg were similarly skewed. Surprisingly, medullary atrophy results from intra-thymic granulocyte infiltration, consequent upon the Th2-mediated autoimmune disease. Dominant tolerance corrects thymic inflammatory disease and loss of thymic function. We demonstrate a reversible RelB-dependent inflammatory mechanism for loss of central tolerance associated with medullary atrophy.
2012-12-27 | GSE43154 | GEO
Project description:Analysis of gene co-expression patterns in TRA-specific medullary thymic epithelial cell (mTEC) subsets. The whole genome gene signatures of purified mTEC subsets respectively positive for the TRAs Gp2, Pdpn, Cea1, Gad1, Ins2, Tspan8 were compared to their corresponding TRA-negative mTEC subset control. Results provide the enriched and depleted gene expressions in the different subsets.
2015-10-28 | GSE69435 | GEO
Project description:Single cell RNA-seq of medullary thymic epithelial cells (mTEC)
| PRJEB33765 | ENA