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Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE89548 | GEO | 2016/11/05

SECONDARY ACCESSION(S): PRJNA352528

REPOSITORIES: GEO

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Excessive expression of miR-27 impairs Treg-mediated immunological tolerance.

Project description:MicroRNAs (miRs) are tightly regulated in the immune system, and aberrant expression of miRs often results in hematopoietic malignancies and autoimmune diseases. Previously, it was suggested that elevated levels of miR-27 in T cells isolated from patients with multiple sclerosis facilitate disease progression by inhibiting Th2 immunity and promoting pathogenic Th1 responses. Here we have demonstrated that, although mice with T cell-specific overexpression of miR-27 harbor dysregulated Th1 responses and develop autoimmune pathology, these disease phenotypes are not driven by miR-27 in effector T cells in a cell-autonomous manner. Rather, dysregulation of Th1 responses and autoimmunity resulted from a perturbed Treg compartment. Excessive miR-27 expression in murine T cells severely impaired Treg differentiation. Moreover, Tregs with exaggerated miR-27-mediated gene regulation exhibited diminished homeostasis and suppressor function in vivo. Mechanistically, we determined that miR-27 represses several known as well as previously uncharacterized targets that play critical roles in controlling multiple aspects of Treg biology. Collectively, our data show that miR-27 functions as a key regulator in Treg development and function and suggest that proper regulation of miR-27 is pivotal to safeguarding Treg-mediated immunological tolerance.

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Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance [Foxp3cre het miR-27Tg]

Project description:MicroRNAs (miRNAs) are tightly regulated in the immune system, as aberrant expression of miRNAs often results in hematopoietic malignancies and autoimmune diseases. Previously, elevated levels of miR-27 in T cells isolated from multiple sclerosis patients has been suggested to facilitate disease progression through inhibiting Th2 immunity and promoting pathogenic Th1 responses. Here we demonstrate that while mice with T cell-specific overexpression of miR-27 harbor dysregulated Th1 responses and develop autoimmune pathology, these disease phenotypes are not driven by miR-27 in effector T cells in a cell-autonomous manner but rather resulted from a perturbed regulatory T (Treg) cell compartment. Excessive miR-27 expression in T cells severely impairs Treg cell differentiation. Moreover, Treg cells with exaggerated miR-27-mediated gene regulation exhibit diminished homeostasis and suppressor function in vivo. Mechanistically, miR-27 represses several known as well as previously uncharacterized targets that play critical roles in controlling multiple aspects of Treg cell biology. Collectively, our data show miR-27 functions as a key regulator in Treg cell development and function and suggest that proper regulation of miR-27 is pivotal to safeguard Treg cell-mediated immunological tolerance.

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Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance [CD4cre miR-23 clusterTg Tr]

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Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance

Project description:Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance

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Classical dendritic cells are required for dietary antigen-mediated peripheral regulatory T cell and tolerance induction

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-28 | E-GEOD-77305 | biostudies-arrayexpress

Aire, guardian of immunological tolerance, binds to and activates super-enhancers

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

2017-01-22 | GSE92654 | GEO

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Project description:Autoimmune regulator (Aire) is a unique transcriptional regulator that induces promiscuous expression of thousands of tissue-restricted antigens (TRAs) in medullary thymic epithelial cells (mTECs), a step critical for induction of immunological self-tolerance. Although several recent studies provided very important molecular insights into how Aire operates, a more comprehensive understanding of this process still remains elusive. Here we demonstrate that a lysine deacetylase Sirtuin-1 (Sirt1) is predominantly expressed in mature Aire+ mTECs, where it is required for expression of Aire-dependent TRA genes and a subsequent induction of immunological self-tolerance. Our study elucidates a previously unknown molecular mechanism for Aire-mediated transcriptional regulation and uncovers a unique functional role for Sirt1 in preventing organ-specific autoimmunity. ~100ng of total RNA isolated by Trizol extraction from MHC-II low and high mTECs (pool of 3 mice) was used to generate poly-A-selected transcriptome libraries using the non-directionnal TruSeq V3 RNA Sample Prep Kit (without additional pre-amplification) following the manufacturer's protocols. Enrichment of DNA fragment with adapter molecules on both ends was done using 15 cycles of PCR amplification using the Illumina PCR mix and primer cocktail. Paired-end (2 × 100 bp) sequencing was performed using the Illumina HiSeq2000 machine.

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Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-08-01 | E-GEOD-83122 | biostudies-arrayexpress