Complement activation and complement receptors in systemic lupus erythematosus.

Abstract

The activation of complement in systemic lupus erythematosus (SLE) was first documented in the early 1950's [52]. Since that time many excellent studies of the biology of complement in SLE have been reported and the general subject has been recently reviewed [3, 13, 49]. In fact, more has been written about the workings of this potent effector pathway in SLE than for any other disease. SLE is characterized serologically by excessive quantities of autoantibodies and immune complexes, and IgG and IgM-bearing immune complexes activate the classical complement pathway. Complement fragments are found on cells and in areas of tissue destruction. Damage to vital tissues in SLE is in part mediated by this effector arm of the humoral immune system. The major observation has been that the characteristic reduction in serum levels of the classical complement pathway components and whole complement activity (THC or CHs0) is secondary to increased utilization [3, 13, 23, 33, 49]. An unexplained observation is that up to 20% of SLE patients also have reduced synthetic rates [1, 43, 50]. Upon reviewing this extensive literature relating to complement and SLE, several clinical points can be made. The measurement of complement components can be helpful adjunct in the initial diagnosis of SLE and is a means of evaluating the results of therapy. For example, if with therapy the complement levels return to normal, the prognosis is better than for patients whose values remain low. These and other data indicate that the more clinically active the disease process, the greater the magnitude of complement activation. These points are well known to students of this illness and will not be further addressed here.