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de Sousa et al., 1988)

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In a mouse model of RA, ROS mediated the tolerance of B cells to autoantigens, and the mutated NCF 1 gene caused ROS deficiency, disrupting resistance to arthritis (89)

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This subsequently activates the key effector caspases caspase-3/7 and cascades to activate caspase-2/6/8/10, ultimately executing apoptosis [41]

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