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Biochim Biophys Acta. 2014 Feb;1843(2):265-74. doi: 10.1016/j.bbamcr.2013.10.020. Epub 2013 Oct 31.

T cell activation induces CuZn superoxide dismutase (SOD)-1 intracellular re-localization, production and secretion.

Author information

1
Dipartimento di Scienze, Università della Basilicata, 85100 Potenza, Italy; Dipartimento di Scienze Mediche Traslazionali, Università di Napoli "Federico II", 80131 Napoli, Italy.
2
Dipartimento di Scienze Mediche Traslazionali, Università di Napoli "Federico II", 80131 Napoli, Italy.
3
Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Napoli, Italy.
4
Dipartimento di Scienze e Tecnologie Ambientali Biologiche e Farmaceutiche, II Università di Napoli, 81100 Caserta, Italy.
5
Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II", 80131 Napoli, Italy.
6
Medicina Clinica e Chirurgia, Università di Napoli "Federico II", 80131 Napoli, Italy. Electronic address: mondola@unina.it.
7
Dipartimento di Scienze Mediche Traslazionali, Università di Napoli "Federico II", 80131 Napoli, Italy. Electronic address: giruggie@unina.it.

Abstract

Reactive oxygen species (ROS) behave as second messengers in signal transduction for a series of receptor/ligand interactions. A major regulatory role is played by hydrogen peroxide (H2O2), more stable and able to freely diffuse through cell membranes. Copper-zinc superoxide dismutase (CuZn-SOD)-1 is a cytosolic enzyme involved in scavenging oxygen radicals to H2O2 and molecular oxygen, thus representing a major cytosolic source of peroxides. Previous studies suggested that superoxide anion and H2O2 generation are involved in T cell receptor (TCR)-dependent signaling. Here, we describe that antigen-dependent activation of human T lymphocytes significantly increased extracellular SOD-1 levels in lymphocyte cultures. This effect was accompanied by the synthesis of SOD-1-specific mRNA and by the induction of microvesicle SOD-1 secretion. It is of note that SOD-1 increased its concentration specifically in T cell population, while no significant changes were observed in the "non-T" cell counterpart. Moreover, confocal microscopy showed that antigen-dependent activation was able to modify SOD-1 intracellular localization in T cells. Indeed, was observed a clear SOD-1 recruitment by TCR clusters. The ROS scavenger N-acetylcysteine (NAC) inhibited this phenomenon. Further studies are needed to define whether SOD-1-dependent superoxide/peroxide balance is relevant for regulation of T cell activation, as well as in the functional cross talk between immune effectors.

KEYWORDS:

Human T lymphocyte; Intracellular localization; Microvesicle secretion; SOD-1; T cell activation; TCR triggering

PMID:
24184207
DOI:
10.1016/j.bbamcr.2013.10.020
[Indexed for MEDLINE]
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