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Initial mitochondrial ROS generation is exacerbated by a plethora of intracellular signaling events, including c-Jun N-terminal kinase activation, leading to an opening of mitochondrial permeability transition pores and the release of endonucleases that cause DNA damage

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As IL-17A was positively linked to IgA while negatively correlating with disease severity markers (Figure 6), consistent with previous reports that IL-17A promoted protective IgA responses (Dann et al., 2015

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Table 1) (Kwong et al., 2012