Interaction Between Glutathione and Apoptosis in Systemic Lupus Erythematosus

Overview

Journal Autoimmun Rev

Publisher Elsevier

Specialty Allergy & Immunology

Date 2013 Jan 3

PMID 23279845

Citations 21

Authors

Dilip Shah

Sangita Sah

Swapan K Nath

Affiliations

Soon will be listed here.

Abstract

Systemic lupus erythematosus (SLE) is characterized by imbalance redox state and increased apoptosis. The activation, proliferation and cell death of lymphocytes are dependent on intracellular levels of glutathione and controlled production of reactive oxygen species (ROS). Changes in the intracellular redox environment of cells, through oxygen-derived free radical production known as oxidative stress, have been reported to be critical for cellular immune dysfunction, activation of apoptotic enzymes and apoptosis. The shift in the cellular GSH-to-GSSG redox balance in favor of the oxidized species, GSSG, constitutes an important signal that can decide the fate of the abnormal apoptosis in the disease. The current review will focus on four main areas: (1) general description of oxidative stress markers in SLE, (2) alteration of redox state and complication of disease, (3) role of redox mechanisms in the initiation and execution phases of apoptosis, and (4) intracellular glutathione and its checkpoints with lymphocyte apoptosis which represent novel targets for pharmacological intervention in SLE.

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