Decreased apoptotic cells (ACs) removal has been described as relevant in systemic lupus erythematosus (SLE) pathogenesis. Binding/phagocytosis of ACs was decreased in SLE patients. Blocking experiments suggested a role for CD36 in ACs clearance in healthy controls, not observed in SLE patients. Binding/phagocytosis of ACs induced the production of IL-6, CXCL8 and CCL22 in patients and controls and IL-1β, TNF-α and CCL3 only in healthy controls. ACs clearance induced an increase in CD80 and a decrease in CD86 expression in healthy controls and atherosclerotic patients. However, SLE patients did not up-regulate CD80 expression. The number and expression of CD36 and CD163 in monocytes was not different between the groups. ACs removal induced a down-regulation of CD36 expression in adherent HLA-DR(+) cells in SLE patients but not healthy controls. The decreased binding/phagocytosis of ACs observed in SLE patients, induces a distinct immune response compared with healthy controls.

中文翻译：

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系统性红斑狼疮患者通过凋亡细胞去除单核细胞活化。

减少的凋亡细胞（ACs）去除已被描述与系统性红斑狼疮（SLE）发病机理有关。SLE患者中AC的结合/吞噬作用降低。阻断实验表明CD36在健康对照中ACs清除中起作用，而在SLE患者中未观察到。AC的结合/吞噬作用诱导了患者和对照中IL-6，CXCL8和CCL22的产生，仅在健康对照中诱导了IL-1β，TNF-α和CCL3的产生。ACs清除在健康对照组和动脉粥样硬化患者中诱导CD80的增加和CD86表达的减少。但是，SLE患者并未上调CD80表达。两组之间单核细胞中CD36和CD163的数量和表达没有差异。AC去除引起SLE患者的粘附HLA-DR（+）细胞中CD36表达的下调，但不影响健康对照组。