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Whole-Cell Recording of Calcium Release-Activated Calcium (CRAC) Currents in Human T Lymphocytes
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Published on: December 21, 2010

Calcium and T lymphocyte activation.

P Gardner1

  • 1Department of Medicine, Stanford University, California 94305.

Cell
|October 6, 1989
PubMed
Summary
This summary is machine-generated.

T cell activation involves a sustained rise in intracellular calcium (Ca2+), crucial for signaling. This study identifies a specific calcium channel in T lymphocytes responsible for this sustained Ca2+ elevation during T cell receptor stimulation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • T cell activation by T cell receptor/CD3 (TCR/CD3) ligands leads to a prolonged increase in intracellular calcium ([Ca2+]i).
  • Calcium (Ca2+) acts as a critical second messenger in early T cell activation, but the downstream molecular events are not fully understood.
  • The [Ca2+]i signal comprises an initial transient peak and a sustained plateau due to altered transmembrane Ca2+ flux.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the sustained elevation of intracellular calcium during T cell activation.
  • To identify the specific ion channels and signaling pathways involved in T cell calcium dynamics.
  • To explore the potential role of G protein-coupled receptors in TCR/CD3-mediated calcium mobilization.

Main Methods:

  • Patch clamp electrophysiology to study Ca2+ permeable channels in T lymphocyte plasma membranes.
  • Analysis of intracellular calcium oscillations and their periodicity.
  • Investigation of feedback mechanisms involving protein kinase C (PKC), phospholipase C (PLC), and other signaling molecules.

Main Results:

  • An inositol trisphosphate (InsP3)-activated, Ca2+-permeable channel in the T cell plasma membrane was identified, likely responsible for sustained [Ca2+]i elevation.
  • TCR/CD3-mediated Ca2+ signaling exhibits repetitive oscillations with a period of 16-20 seconds, suggesting frequency-encoded signaling.
  • Multiple nonlinear feedback loops, including PKC-mediated CD3 gamma phosphorylation and Ca2+-dependent PLC activation, contribute to the oscillatory Ca2+ signal.

Conclusions:

  • A specific plasma membrane calcium channel is crucial for sustained Ca2+ signaling in T cell activation.
  • The oscillatory nature of the Ca2+ signal suggests a complex frequency-modulated signaling system.
  • Further research is needed to elucidate the precise role of G proteins and the structural homology of TCR/CD3 to G protein-coupled receptors in T cell activation.