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  4. Study on redox status, mitochondrial function and cationic ion transport in immume-related cells in Patients with SLE
 
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Study on redox status, mitochondrial function and cationic ion transport in immume-related cells in Patients with SLE

Date Issued
2005
Date
2005
Author(s)
Chang, Chia-Chee
DOI
zh-TW
URI
http://ntur.lib.ntu.edu.tw//handle/246246/51344
Abstract
The systemic lupus erythematosus (SLE) is a main disease of the immune disease. Patients of SLE suffer from various kinds of organs. In addition, it will also have serious influence on the increase of infection, and this is the main pathogenic and cause of death of the disease, too. Susceptibility to common and opportunistic infections is a major cause of morbidity and mortality in these patients.The important factor of this is the functional defects of the immune cells per se. It is well recognized that hyporesponsiveness to stimulation are found in both polymorphonuclear neutrophils (PMN) and mononuclear cells (MNC) of patients with active SLE. In previous reports demonstrated that SLE-PMN was not only defective in IL-8 production but hyporesponsive to IL-8 stimulation. On the other hand, hyporesponsiveness/anergy of SLE-MNC to phytomitogens, specific antigens, allogeneic and autologous cells stimulation were documented in vitro. However, the real cause for SLE-MNC hyporesponsiveness has not been elucidated yet. Recently, many authors have identified a number of aberrated antigen receptor-mediated signal events in T and B lymphocytes from patients with active SLE. Although the TCR- or BCR-mediated increases in protein tyrosine phosphorylation and cytoplasmic free Ca2+, along with T cell receptor zeta chain deficiency is consistent with the presence of active cells in vivo. But this can not explain the defective responsiveness of SLE-MNC to common antigens such as tetanus toxoid in vitro. It is now quite clear that many biological molecules that are critically important in signaling and in the regulation of gene expression are sensitive cell to reactive oxygen species (ROS) at a concentration much lower than require inflict oxidative damage. Oxidation-reduction (redox) based regulation of signal transduction and gene expression is emerging as a fundamental regulatory mechanism in cell biology. A low, physiological concentration of ROS can regulate a variety of key molecular mechanisms linking with immune responses, cell-cell adhesion, cell proliferation, inflammation, metabolism, aging and death.. Based on these facts,we hypothesized that the hyporesponsiveness of MHC and PMN to stimulation signaling in patients with SLE is related to imbalanced redox state.However, more investigations are needed to solve it. This main purpose of this experiment is to study the possible cause of hyporesponsiveness in systemic lupus erythematosus.
Subjects
紅斑性狼瘡
redox status
Type
other
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ntu-94-P88448006-1.pdf

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