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Related Concept Videos

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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.
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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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A Distinct Inhibitory Function for miR-18a in Th17 Cell Differentiation.

Misty M Montoya1, Julia Maul2, Priti B Singh1

  • 1Department of Microbiology and Immunology, Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143.

Journal of Immunology (Baltimore, Md. : 1950)
|June 14, 2017
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MicroRNA-18a (miR-18a) limits T helper 17 (Th17) cell differentiation. Inhibiting miR-18a enhances Th17 cell development, impacting immunity and autoimmune diseases.

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Area of Science:

  • Immunology
  • Molecular Biology
  • MicroRNA Regulation

Background:

  • T helper 17 (Th17) cells are crucial for immunity against extracellular pathogens.
  • Dysregulated Th17 cell responses are implicated in autoimmune disease pathogenesis.
  • MicroRNAs (miRNAs) are key regulators of cellular differentiation and function.

Purpose of the Study:

  • To investigate the role of microRNA-18a (miR-18a) in regulating Th17 cell differentiation.
  • To identify the molecular targets of miR-18a involved in the Th17 cell pathway.

Main Methods:

  • Analysis of miRNA expression in activated T cells.
  • In vitro differentiation assays of Th17 cells with miR-18a modulation.
  • In vivo studies using airway inflammation models.
  • Inhibition of miR-18a in mouse and human CD4+ T cells.
  • Bioinformatic analysis to predict and validate miR-18a targets.

Main Results:

  • miR-18a was significantly upregulated in activated T cells.
  • miR-18a deficiency led to enhanced Th17 cell differentiation and increased IL-17A production in vitro and in vivo.
  • Inhibition of miR-18a increased Th17 cell markers (CCR6, RORγt) in both mouse and human T cells, indicating functional conservation.
  • miR-18a directly targets key Th17 transcription factors: Smad4, Hif1a, and Rora.

Conclusions:

  • miR-18a acts as a critical negative regulator of Th17 cell differentiation.
  • The miR-17-92 cluster, through miR-18a, fine-tunes Th17 cell development.
  • Targeting miR-18a may offer therapeutic strategies for Th17-mediated inflammatory and autoimmune diseases.