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Considerable evidence supports the role of a deregulated clearance of dying cells in the pathogenesis of lupus. The dissection of this event in mouse models has provided insight into the origin and persistence of the autoantibodies, which represent a hallmark of the disease, and other processes critical for chronic inflammation and tissue damage. The comparison with animals that do not develop autoimmunity has also led to the identification of specific events in the pathway to lupus. Recent advances have provided evidence for the feasibility of rational therapeutic procedures, aimed at preventing immune-mediated damage and restoring tissue homeostasis.
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Rovere‐Querini et al. (2006) studied this question.
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