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Third, lack of HO-1 expression in bone marrow-derived cells resulted in atherosclerotic plaques with a larger inflammatory component, suggestive of greater vulnerability for rupture (Orozco et al., 2007)

Supervision was contributed by EC, SM, MD, AD, TC, DL, GC, CL, VM, RG, FP, FCi, KA, and LB

Such an increase in MDA-modified proteins, anti-SOD, and anti-catalase antibodies in SLE patients induces oxidative stress with the onset of the disease ( Interestingly, these ROS indicators of oxidative damage can be considered for the development of biomarkers ( 4 Armory of immune cells dysregulating SLE 4.1 Functional influence of T cells and B cells in SLE T cells play a major role in the initiation of SLE, and uncontrollably activated B cells are produced by T-cell dysregulation, which impacts peripheral immune tolerance

Ther Apher (2000) 4:2759

However, there remain certain limitations in this study: 1) Due to the formatting requirements of Citespace, the analysis was conducted only on literature retrieved from WoSCC, and other databases such as PubMed and Scopus were not included

Finally, excessive ROS production may lead to dysregulated T-cell homeostasis by differential modulation of T-cell homeostasis as effector T cells are more susceptible to ROS-mediated cell death than Tregs [201, 315, 316]
