14 - Immune complexes

Abstract

Systemic lupus erythematosus (SLE) is the prototype of human diseases that are principally mediated by immune complexes. The evidence for tissue injury by immune complexes in SLE is marshaled from many observations. The recognition of a number of autoantibodies in this disease served as an important initial finding. The presence of immunoglobulin and complement deposits in target organs and the characteristics of pathologic changes allowed the comparison of SLE to experimental models of serum sickness. The conclusive evidence of the involvement of immune complexes in the genesis of tissue lesions, however, was provided by the identification of specific antibodies in the glomeruli of patients with SLE. Injury to specific target organs in immune complex-mediated diseases results from the presence of antigen–antibody complexes in tissue. Immune complex deposits activate complement and interact with cell receptors, leading to the release of cytokines from cells and culminating in tissue damage and organ dysfunction. Antigen–antibody deposits in tissue may arise from deposition in tissues of circulating immune complexes, from formation of immune complexes at the site of their existence in tissues, or a combination of both. This chapter reviews the nature of immune complexes, considers the biologic properties of immune complexes in relation to pathogenic processes, and discusses the clinical application of tests for the detection of immune complexes.