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Hnf4 controls gut and liver gene programs in the thymus [bulk_RNAseq]

ABSTRACT: We profiled medullary thymic epithelial cells by bulk RNA-seq to investigate mechanisms of T-cell tolerance.

ORGANISM(S): Mus musculus

PROVIDER: GSE225659 | GEO | 2023/06/26

REPOSITORIES: GEO

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Hnf4 controls gut and liver gene programs in the thymus [scRNAseq]

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Hnf4 controls gut and liver gene programs in the thymus

Project description:This SuperSeries is composed of the SubSeries listed below.

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Hnf4 controls gut and liver gene programs in the thymus [bulk_RNAseq]

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Thymic epithelial cells co-opt lineage-defining transcription factors to eliminate autoreactive T cells [RNA-seq]

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Comparison of RelB-/- and RelB+/- thymi

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. VÎ² 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

Hnf4 controls gut and liver gene programs in the thymus

Project description:Hnf4 controls gut and liver gene programs in the thymus

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Single cell RNA sequencing of thymic dendritic cells reveals molecular determinants of antigen transfer in the thymus

Project description:The presentation of self-antigens in the thymus by medullary thymic epithelial cells (mTECs) and dendritic cells (DCs) is crucial for the establishment of central tolerance. While mTECs produce and present self-antigens in an autonomous manner, DCs acquire them from mTECs by Cooperative Antigen Transfer (CAT). Although CAT represents a key process of central tolerance, molecular determinants which drive CAT are largely unknown. To reveal these determinants, we compared the transcriptomes of CAT-experienced and CAT-inexperienced DCs via scRNAseq. Specifically, we sequenced TdTOMATO+ and TdTOMATO– CD11c+ and CD11b+ cells from the thymus of Foxn1CreR26TdTOMATO mice. In this model, fluorescent TdTOMATO protein is exclusively produced by thymic epithelium, thus TdTOMATO expression in DCs (CD11c+ and CD11b+ cells) mark their previous experience of CAT. Using this approach we unraveled several candidate determinants of CAT. We focused on the gene determinant, Cldn1, encoding the tight junction protein Claudin 1, that was found to be highly expressed among the CAT-experienced type 1 lineage DCs. We performed further experiments that confirmed its role in driving CAT. In addition, this scRNAseq approach allowed us to redefine the heterogeneity and maturation states of thymic DCs.

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Comparison of RelB-/- and RelB+/- thymi

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