Decreased levels of complement components, including C3, C4, and CH50, is one of the characteristic laboratory parameters of SLE that also correlates with disease activity. C3b, derived from C3 by either the classic or alternative pathway of complement activation, provides a binding site for C5, making it susceptible to the action of C5 convertase. This activity triggers the terminal sequence of complement activation that leads to membrane damage (Moxley and Ruddy 1997). A monoclonal antibody designed to interfere with C5 activity decreased proteinuria and improved survival in treated NZB/NZW mice (Matis and Rollins 1995, Strand 2000). Moreover, in a singlesite, dose-finding, phase I trial, 24 patients with SLE have been treated with a humanized anti-C5 monoclonal antibody (5G1.1), and a phase II trial is under way. However, the results of these trials are not yet available.

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