Nitric oxide, mitochondrial hyperpolarization, and T cell activation

Gyorgy Nagy, Agnes Koncz, David Fernandez, Andras Perl

Research output: Contribution to journalReview article

51 Citations (Scopus)

Abstract

T lymphocyte activation is associated with nitric oxide (NO) production, which plays an essential role in multiple T cell functions. NO acts as a messenger, activating soluble guanyl cyclase and participating in the transduction signaling pathways involving cyclic GMP. NO modulates mitochondrial events that are involved in apoptosis and regulates mitochondrial membrane potential and mitochondrial biogenesis in many cell types, including lymphocytes. Mitochondrial hyperpolarization (MHP), an early and reversible event during both activation and apoptosis of Tlymphocytes, is regulated by NO. Here, we discuss recent evidence that NO-induced MHP represents a molecular switch in multiple T cell signaling pathways. Overproduction of NO in systemic lupus erythematosus induces mitochondrial biogenesis and alters Ca2+ signaling. Thus, whereas NO plays a physiological role in lymphocyte cell signaling, its overproduction may disturb normal T cell function, contributing to the pathogenesis of autoimmunity.

Original languageEnglish
Pages (from-to)1625-1631
Number of pages7
JournalFree Radical Biology and Medicine
Volume42
Issue number11
DOIs
Publication statusPublished - Jun 1 2007

    Fingerprint

Keywords

  • Apoptosis
  • Calcium
  • Free radicals
  • Mitochondrial biogenesis
  • Mitochondrial hyperpolarization
  • Nitric oxide

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

Cite this