Oxidative Stress in SLE T Cells, Is NRF2 Really the Target to Treat?
1Department of Pediatrics, Pediatric Rheumatology, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Abstract:
Oxidative stress is a major component of cellular damage in T cells from patients with systemic lupus erythematosus (SLE) resulting amongst others in the generation of pathogenic Th17 cells. The NRF2/Keap1 pathway is the most important antioxidant system protecting cells from damage due to oxidative stress. Activation of NRF2 therefore seems to represent a putative therapeutic target in SLE, which is nevertheless challenged by several findings suggesting tissue and cell specific differences in the effect of NRF2 expression. This review focusses on the current understanding of oxidative stress in SLE T cells and its pathophysiologic and therapeutic implications.
Insights
Systemic lupus erythematosus (SLE) involves T cell damage from oxidative stress, creating harmful Th17 cells. Targeting the NRF2/Keap1 antioxidant pathway may treat SLE, but requires understanding cell-specific effects.
Area of Science:
- Immunology and Molecular Medicine
- Cellular Biology
- Autoimmune Diseases
Background:
- Oxidative stress significantly damages T cells in patients with systemic lupus erythematosus (SLE).
- This cellular damage contributes to the development of pathogenic T helper 17 (Th17) cells.
- The Nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1 (Keap1) pathway is crucial for cellular defense against oxidative stress.
Purpose of the Study:
- To review the current understanding of oxidative stress in T cells within the context of SLE.
- To explore the pathophysiological role of oxidative stress and the NRF2/Keap1 pathway in SLE.
- To discuss the therapeutic implications of targeting the NRF2/Keap1 pathway for SLE treatment.
Main Methods:
- Literature review of studies on oxidative stress in SLE T cells.
- Analysis of the NRF2/Keap1 pathway's role in cellular protection and its relevance to SLE.
- Examination of evidence regarding cell-specific and tissue-specific effects of NRF2 modulation.
Main Results:
- Oxidative stress is a key factor in T cell dysfunction and pathogenesis in SLE.
- The NRF2/Keap1 pathway is a critical endogenous antioxidant system.
- Potential therapeutic targeting of NRF2 in SLE is complicated by context-dependent effects.
Conclusions:
- Understanding oxidative stress in SLE T cells is vital for developing effective therapies.
- The NRF2/Keap1 pathway presents a promising therapeutic target, but its precise role requires further investigation.
- Cell- and tissue-specific differences in NRF2 activity must be considered for successful SLE treatment strategies.
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