ABSTRACT
The role of complement in human autoimmune disease is multifaceted, and its involvement in pathogenesis varies from disease to disease. Complement’s participation in autoimmunity is most obvious in systemic antibody-mediated diseases complicated by accumulation and deposition of immune complexes (ICs), of which systemic lupus erythematosus (SLE) is the prototype. Organ-specific diseases that seem to have only monoclonal or oligoclonal autoantibody expansion, such as thyroiditis or myasthenia gravis, and T cell-mediated diseases, such as diabetes mellitus and multiple sclerosis, have not yet been causally linked with abnormalities in the complement system.
