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Related Concept Videos

Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
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TCR down-regulation controls virus-specific CD8+ T cell responses.

Charlotte Menné Bonefeld1, Mariëlle Haks, Bodil Nielsen

  • 1Department of International Health, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.

Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 2008
PubMed
Summary

The CD3gamma motif is crucial for T cell receptor (TCR) regulation. Its mutation impairs virus-specific CD8(+) T cell expansion by increasing apoptosis, highlighting its role in immune response.

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Area of Science:

  • Immunology
  • T cell biology
  • Virology

Background:

  • The CD3gamma di-leucine-based motif is known to be involved in T cell receptor (TCR) down-regulation.
  • The precise role of this motif in physiological T cell responses remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function of the CD3gamma di-leucine-based motif in the context of virus-specific T cell responses.
  • To elucidate the molecular mechanisms by which CD3gamma influences T cell expansion during viral infections.

Main Methods:

  • Utilized genetically modified mice with a mutated CD3gamma di-leucine-based motif.
  • Assessed the expansion of virus-specific CD8(+) T cells following infection with vesicular stomatitis virus and lymphocytic choriomeningitis virus.
  • Analyzed early TCR signaling, T cell recruitment, proliferation, apoptosis rates, and Bcl-2 expression.

Main Results:

  • Mice with mutated CD3gamma exhibited impaired expansion of virus-specific CD8(+) T cells.
  • The mutation did not affect early TCR signaling, recruitment, or proliferation but increased apoptosis.
  • Increased apoptosis was linked to enhanced down-regulation of the antiapoptotic molecule Bcl-2, leading to a 2-fold reduction in clonal expansion.

Conclusions:

  • The CD3gamma di-leucine-based motif is essential for the clonal expansion of virus-specific CD8(+) T cells.
  • CD3gamma-mediated TCR down-regulation plays a critical role in controlling T cell apoptosis and ensuring robust viral immunity.
  • This study identifies a key regulatory mechanism governing T cell responses during viral infections.