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Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

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Retroviral Transduction of Helper T Cells as a Genetic Approach to Study Mechanisms Controlling their Differentiation and Function
11:50

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Published on: November 4, 2016

MicroRNA 10a marks regulatory T cells.

Lukas T Jeker1, Xuyu Zhou, Kseniya Gershberg

  • 1Diabetes Center and the Department of Medicine, University of California San Francisco, San Francisco, California, United States of America.

Plos One
|May 26, 2012
PubMed
Summary

MicroRNA-10a (miR-10a) is selectively expressed in regulatory T cells (Tregs). Lower miR-10a levels correlate with autoimmune diabetes susceptibility and Treg instability, though its genetic absence shows complex effects on FoxP3 expression.

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Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) are key regulators of T cell function and stability.
  • Regulatory T cells (Tregs) are crucial for immune homeostasis and preventing autoimmunity.
  • Dysregulation of Tregs is implicated in autoimmune diseases like diabetes.

Purpose of the Study:

  • To investigate the role of microRNA-10a (miR-10a) in regulatory T cell (Treg) stability and function.
  • To compare miR-10a expression in Tregs between autoimmune-prone and resistant mouse models.
  • To assess the impact of miR-10a modulation on Treg phenotype and FoxP3 expression.

Main Methods:

  • Expression profiling of miR-10a in different T cell subsets and mouse strains (NOD vs. C57BL/6J).
  • In vitro inhibition of miR-10a using antagomiRs and assessment of FoxP3 levels.
  • Genetic ablation of miR-10a in mice.
  • Analysis of Treg number, phenotype, and FoxP3 induction capacity under various conditions (TGF-β, RA).

Main Results:

  • miR-10a is selectively expressed in Tregs, not other T cells.
  • NOD mice exhibit lower Treg-specific miR-10a expression compared to resistant C57BL/6J mice.
  • In vitro miR-10a inhibition reduces FoxP3 levels; lower miR-10a is found in unstable 'exFoxP3' T cells.
  • Retinoic acid (RA) induces miR-10a in TGF-β-induced iTregs, suggesting a role in stability.
  • Genetic ablation of miR-10a did not alter natural Treg numbers/phenotype or conventional T cell FoxP3 induction.

Conclusions:

  • miR-10a is selectively expressed in Tregs and its expression is reduced in autoimmune-prone mice.
  • While miR-10a inhibition impacts FoxP3 in vitro, genetic ablation yields discordant effects, indicating a complex regulatory role.
  • Further research is needed to fully elucidate miR-10a's function in Treg stability and autoimmune disease pathogenesis.