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Editorial
. 2012 Mar;142(3):219-22.
doi: 10.1016/j.clim.2011.12.011. Epub 2011 Dec 30.

Oxidative stress and endosome recycling are complementary mechanisms reorganizing the T-cell receptor signaling complex in SLE

Andras Perl
Editorial

Oxidative stress and endosome recycling are complementary mechanisms reorganizing the T-cell receptor signaling complex in SLE

Andras Perl. Clin Immunol. 2012 Mar.
No abstract available

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Figures

Figure 1
Figure 1
Schematic diagram of the metabolic pathways regulating oxidative stress and endosome traffic controlling the recycling of receptor and adaptor proteins between the cell surface and lysosomes. The pentose phosphate pathway (PPP), reduced glutathione (GSH), and nitric oxide (NO) regulate mitochondrial electron transport, the transmembrane potential (Δψm) and the production of reactive oxygen intermediates. The mammalian target of rapamcyin (mTOR) senses Δψm and regulates endosome traffic, protein homeostasis through balancing translation and lysosomal degradation via autophagy. Necrosis-prone T cells release oxidized DNA and HMGB1 which stimulate macrophages, and dendritic cells to produce NO and interferon alpha (IFN-α). Oxidation of cysteine residues and endocytic recycling are proposed to mediate the depletion of the linker for activation of T cells (LAT) in lipid rafts of T lymphocytes in patients with SLE.
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