Single cell RNA-seq analysis of mature thymic epithelial cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE60297 | GEO | 2014/09/04
SECONDARY ACCESSION(S): PRJNA257979
REPOSITORIES: GEO
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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: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.
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Project description:We used Affymetrix microarrays to understand the genome wide differences in Adult and fetal cortical thymic epithelial cells (cTEC) and medullary thymic epithelial cells (mTEC)
2017-02-10 | GSE81433 | GEO
Project description:10x sequencing of TSPAN8+, GP2+ or Unselected medullary thymic epithelial cells (mTEC) isolated from female C57BL/6, BALB/c, and C57BL/6 x BALB/c F1 mice with the intent to identify co-expression patterns in promiscuously expressed genes in individual mTEC.
2019-10-17 | E-MTAB-8105 | biostudies-arrayexpress
Project description:Medullary thymic epithelial cells play essential role for induction of central self-tolerance by facilitating negative selection of self-reactive thymocytes and the generation of Foxp3+ regulatory T cells. Although studies highlighted the non-canonical NFκB pathway as the key regulator of mTEC development, comprehensive understanding of the molecular pathways regulating this process still remains incomplete. The aim of this study was to analyze the impact of Histone deacetylase 3 (HDAC3), which is highly expressed by mTECs, on mTEC development and function. We used Affymetrix mouse 1ST arrays to analyze the impact of the Hdac3 gene on the gene expression profile of MHC-II medullary thymic epithelial cells
2016-04-01 | GSE78283 | GEO
Project description:Thymic epithelial cells (TECs) support T cell development in the thymus. Cortical thymic epithelial cells (cTECs) facilitate positive selection of developing thymocytes whereas medullary thymic epithelial cells (mTECs) facilitate the deletion of self-reactive thymocytes in order to prevent autoimmunity. The mTEC compartment is highly dynamic with continuous maturation and turnover, but the genetic regulation of these processes remains poorly understood. MicroRNAs (miRNAs) are important regulators of TEC genetic programs since miRNA-deficient TECs are severely defective. However, the individual miRNAs important for TEC maintenance and function and their mechanisms of action remain unknown. Here, we demonstrate that miR-205 is highly and preferentially expressed in mTECs during both thymic ontogeny and in the postnatal thymus. This distinct expression is suggestive of functional importance for TEC biology. Genetic ablation of miR-205 in TECs, however, neither revealed a role for miR-205 in TEC function during homeostatic conditions nor during recovery from thymic stress conditions. Thus, despite its distinct expression, miR-205 on its own is largely dispensable for mTEC biology. In order to identify miRNAs differentially expressed in mTECs, we purified cortical thymic epithelial cells (cTECs), mTECs and CD45+ cells as three distinct populations and prepared RNA for microarray analysis. Thymic subsets were FACS-purified from 4-week old NOD wildtype mice. Thymi from 10-12 female mice were pooled together for stromal cell isolation for a total of 3 CD45+, 2 cTEC and 3 mTEC biologic replicates.
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Project description:Thymic epithelial cells (TEC) effect crucial roles in thymopoiesis including the control of negative thymocyte selection. This process depends on their capacity to express promiscuously genes encoding tissue-restricted antigens. This competence is accomplished in medullary TEC (mTEC) in part by the presence of the transcriptional facilitator AutoImmune REgulator, AIRE. AIRE-regulated gene transcription is marked by repressive chromatin modifications, including H3K27me3. When during TEC development these chromatin marks are established, however, remains unclear. Here we use a comprehensive ChIP-seq dataset of multiple chromatin modifications in different TEC subtypes to demonstrate that the chromatin landscape is established early in TEC differentiation. Much of the chromatin architecture found in mature mTEC was found to be present already over earlier stages of mTEC lineage differentiation. This was reflected by the fact that a machine learning approach accurately classified genes as AIRE-induced or AIRE-independent both in immature and mature mTEC. Moreover, analysis of TEC specific enhancer elements identified candidate transcription factors likely to be important in mTEC development and function. Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.
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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:Thymic epithelial cells (TECs) are a critical functional component of the thymus’s ability to generate T cells for the adaptive immune system in vertebrates. However, no in vitro system for studying TEC function exists. Overexpressing the transcription factor FOXN1 initiates transdifferentiation of fibroblasts into TEC-like cells (iTECs) that support T cell differentiation in culture or after transplant. In this study, we characterized iTEC programming at the cellular and molecular level to determine how it proceeds and identified mechanisms that can be targeted for improving this process. These data showed that iTEC programming consisted of discrete gene expression changes that differed early and late in the process, and that iTECs upregulated markers of both cortical and medullary TEC (cTEC and mTEC) lineages. We demonstrated that promoting proliferation enhanced iTEC generation, and that Notch inhibition allowed induction of mTEC differentiation. Finally, we showed that MHCII expression was the major difference between iTECs and fetal TECs. MHCII expression was improved by co-culturing iTECs with fetal double-positive T-cells. This study supports future efforts to improve iTEC generation for both research and translational uses.
2024-04-22 | GSE264266 | GEO
Project description:Thymic epithelial cells (TECs) are a critical functional component of the thymus’s ability to generate T cells for the adaptive immune system in vertebrates. However, no in vitro system for studying TEC function exists. Overexpressing the transcription factor FOXN1 initiates transdifferentiation of fibroblasts into TEC-like cells (iTECs) that support T cell differentiation in culture or after transplant. In this study, we characterized iTEC programming at the cellular and molecular level to determine how it proceeds and identified mechanisms that can be targeted for improving this process. These data showed that iTEC programming consisted of discrete gene expression changes that differed early and late in the process, and that iTECs upregulated markers of both cortical and medullary TEC (cTEC and mTEC) lineages. We demonstrated that promoting proliferation enhanced iTEC generation, and that Notch inhibition allowed induction of mTEC differentiation. Finally, we showed that MHCII expression was the major difference between iTECs and fetal TECs. MHCII expression was improved by co-culturing iTECs with fetal double-positive T-cells. This study supports future efforts to improve iTEC generation for both research and translational uses.
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