Concluding remarks

A deep insight into the complex genetic structure of most complement components and their evolution has been gained in the last decade. A number of genetic abnormalities of complement components have been observed in association with disease. It is, however, still premature to bridge the variation or loss of in vitro functions to a given in vivo situation. It will be an important task to replace the statistical relationship of a disease association by the eluci dation of causal factors in the pathogenesis of com-plement-related diseases, as well as to establish evidence for a functional relevance of polymorphic complement allotypes in the natural selection process.

See also: Complement, alternative pathway; Complement, classical pathway; Complement deficiencies; Complement receptors; Decay-accelerating factor (CD55); H2 class III; HLA class III region; Systemic lupus erythematosus (SLE), human.

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