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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Dicer controls CD8+ T-cell activation, migration, and survival.

Nu Zhang1, Michael J Bevan

  • 1Department of Immunology and The Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 25, 2010
PubMed
Summary

Dicer enzyme deletion in mature CD8(+) T cells enhances early activation but impairs pathogen response and accumulation. MicroRNAs regulate CD69 expression, crucial for T cell migration and survival.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Dicer enzyme is essential for microRNA production.
  • The role of Dicer and microRNAs in mature CD8(+) T cells remains largely unexamined.
  • CD8(+) T cells are critical for adaptive immunity.

Purpose of the Study:

  • To investigate the function of Dicer in mature CD8(+) T cells.
  • To determine the impact of Dicer deletion on T cell activation, proliferation, and in vivo function.
  • To identify microRNAs regulating CD69 expression in activated T cells.

Main Methods:

  • Dicer deletion in mature CD8(+) T cells using tat-cre or distal lck promoter.
  • Antigenic challenge with pathogen infection in vivo.
  • In vitro T cell activation assays using anti-CD3 and anti-CD28 stimulation.
  • Analysis of CD69 expression and T cell migration.
  • Identification of microRNAs targeting CD69 mRNA 3'UTR.

Main Results:

  • Dicer-deleted CD8(+) T cells showed accelerated early activation (CD69 upregulation, earlier mitosis) in vitro.
  • Dicer-deleted CD8(+) T cells failed to accumulate effectively during in vivo pathogen response.
  • Sustained CD69 expression in Dicer-deleted T cells led to defective migration from lymphoid organs.
  • miR-130/301 were identified as key microRNAs downregulating CD69 expression post-activation.

Conclusions:

  • Dicer-dependent microRNA functions are dispensable for initial CD8(+) T cell activation.
  • Dicer-mediated microRNA production is essential for CD8(+) T cell survival, accumulation, and proper migration during an immune response.
  • MicroRNA regulation of CD69 is critical for controlling T cell egress from lymphoid tissues.