Elevated CRP levels also boosted macrophage uptake of apoptotic cells and sustained anti-inflammatory TGF-β expression; however, in the absence of C1q, CRP failed to suppress proinflammatory TNF-α and may therefore even exacerbate inflammation, emphasizing the importance of C1q and CRP working together to ensure non-inflammatory clearance of dying cells and suggesting a mechanism linking deficiencies in early complement components and CRP to autoimmune diseases such as SLE. Here, CRP is linked to systemic lupus erythematosus.