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Abstract
Rheumatoid Arthritis (RA) is an autoimmune disease with uncertain pathophysiology involving many interwoven signalling cascades. ROS, NK and NKT cells might be crucial in the disease severity of RA. However, the role of oxidative stress, its impact on NK and NKT cell immunobiology and disease activity (DAS28) is largely unknown.
Highlights
Rheumatoid Arthritis (RA) is an autoimmune disease with uncertain pathophysiology involving many interwoven signalling cascades
Results explained a state of profound oxidative stress in the peripheral blood of RA patients
The depolarized mitochondrial membrane potential, FAS, FASL and active caspase-3 positive NK and NKT cell subsets were much elevated in patients
Summary
Rheumatoid Arthritis (RA) is an autoimmune disease with uncertain pathophysiology involving many interwoven signalling cascades. ROS, NK and NKT cells might be crucial in the disease severity of RA. The role of oxidative stress, its impact on NK and NKT cell immunobiology and disease activity (DAS28) is largely unknown. Aim In this study, we assessed the role of oxidative stress and NK cell subsets in the disease pathogenesis of RA
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