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Modulation of intracellular Cl- homeostasis by lectin-stimulation in Jurkat T lymphocytes

Zhong-Fang Lai1, Yu-Zhen Chen, Katsuhide Nishi

  • 1Department of Cell and Biological Pharmacology, Graduate School of Medical Sciences, Kumamoto University, Honjo 1-1-1, Kumamoto 860-0811, Japan. lai-zf@gpo.kumamoto-u.ac.jp

European Journal of Pharmacology
|December 9, 2003
PubMed

Insights

Lectin stimulation increases intracellular chloride concentration ([Cl(-)](i)) and oscillations in Jurkat T cells, crucial for their activation and proliferation. This chloride ion flux is mediated by Cl(-) channels.

Area of Science:

  • Immunology
  • Cell Biology
  • Physiology

Background:

  • T lymphocyte activation and proliferation are complex processes involving various signaling pathways.
  • Intracellular ion concentrations, particularly chloride, play a role in cell signaling and function.
  • Jurkat T lymphocytes are a widely used model system for studying T cell activation.

Purpose of the Study:

  • To investigate the role of intracellular chloride concentration ([Cl(-)](i)) changes during lectin-induced activation and proliferation in human Jurkat T lymphocytes.
  • To determine the mechanisms underlying lectin-induced chloride ion flux and its impact on T cell responses.
  • To explore the involvement of chloride channels and oscillations in T cell activation and proliferation.

Main Methods:

  • Measurement of intracellular chloride concentration ([Cl(-)](i)) using the MQAE fluorescence dye.
  • Stimulation of Jurkat T lymphocytes with lectins (phytohemagglutinin, concanavalin A) and mitochondrial metabolism inhibitors (CCP, 2,4-dinitrophenol).
  • Assessment of chloride channel activity using anthracene-9-carboxylate (9-AC) and manipulation of extracellular chloride levels.

Main Results:

  • Lectins dose-dependently increased [Cl(-)](i) and triggered intracellular chloride oscillations.
  • Mitochondrial metabolism inhibitors increased [Cl(-)](i) but did not induce oscillations.
  • Inhibition of chloride channels and removal of extracellular chloride blocked lectin-induced increases in [Cl(-)](i) and Jurkat T cell proliferation.

Conclusions:

  • Elevation of intracellular chloride concentration ([Cl(-)](i)) via chloride channel activation is essential for lectin-induced Jurkat T cell proliferation.
  • Intracellular chloride oscillations may play a significant role in modulating T cell activation and proliferation.
  • Targeting chloride channels could be a potential strategy for modulating T cell responses.

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