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Cellular signaling in thymocyte apoptosis.

D J McConkey1, M Jondal, S Orrenius

  • 1Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, MA 02115.

Seminars in Immunology
|December 1, 1992
PubMed
Summary

T cell receptor triggering induces apoptosis (programmed cell death) in thymocytes. Signal transduction pathways like calcium, cAMP, and protein kinase C regulate this cell death during T cell development.

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Area of Science:

  • Immunology
  • Cell Biology
  • Developmental Biology

Background:

  • Apoptosis, or programmed cell death, is crucial for T cell development in the thymus.
  • T cell receptor (TCR) triggering is implicated in negative selection, a process involving cell death.

Purpose of the Study:

  • To investigate the regulatory mechanisms of apoptosis in thymocytes upon TCR triggering.
  • To understand how signal transduction pathways influence TCR-mediated cell death in T cells.

Main Methods:

  • Examining the role of cytosolic Ca2+ levels and cAMP in thymocyte apoptosis.
  • Investigating the effects of protein kinase C (PKC) activation on apoptosis.
  • Analyzing the impact of co-stimulatory molecule crosslinking (Thy-1, CD4, CD8) on TCR-mediated cell death.
  • Assessing the involvement of protein tyrosine kinases in these processes.

Main Results:

  • Elevated cytosolic Ca2+ and increased cAMP levels can trigger thymocyte apoptosis.
  • Protein kinase C activation appears to inhibit apoptosis induced by Ca2+ or cAMP.
  • Crosslinking of Thy-1, CD4, or CD8 potentiates TCR-mediated cell death, involving protein tyrosine kinases.

Conclusions:

  • Signal transduction pathways significantly regulate apoptosis during thymocyte development.
  • TCR occupancy can mediate both T cell differentiation and programmed cell death.
  • Understanding these pathways is key to comprehending intrathymic T cell development.

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