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NETs are characterized by large, web-like structures composed of chromatin, histones, and proteins ( Figure 3 Low-density granulocytes (LDGs), a pro-inflammatory neutrophil subset, drive spontaneous NET release that induces endothelial dysfunction and vascular injury in SLE-associated AS ( NETs further sustain vascular inflammation via macrophage inflammasome activation and IL-18-driven NETosis ( 2.4 T-cell dysfunction T-cell dysfunction is essential in the development of AS in SLE patients, as shown in Figure 4

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