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About Autoantibodies

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Overview of Autoimmunity
Autoimmune diseases

While mechanisms of self-tolerance normally protect an individual from potentially self-reactive lymphocytes, there are failures. They result in an inappropriate response of the immune system against self-components termed autoimmunity.

Autoimmune disease include more than 70 different disorders affecting approximately 5% of the population of the western countries. A large number of serum antibodies directed against functional structures of the cell (nucleic acid, nuclear molecules, receptors, or other functional cell components) can be detected in human autoimmune diseases; its presence plays a central role in the diagnosis and classification of this type of disorders. Moreover, several longitudinal cohort studies have shown that patients may carry autoantibodies many years before they manifest clinical symptoms and detecting these antibodies in serum has been shown to have strong predictive value. Despite the growing knowledge of immunology during the past decades, more than one challenge regarding autoantibodies remains open, such as determining the mechanism involved in the breakdown of tolerance as well as identifying the nature of the autoimmune damage mediated by many of them.

The detection of autoantibodies in several conditions was the first element that supported the role of the immune system in these autoimmune diseases. As antibodies were already well-known effector molecules, the definition of pathogenic mechanisms for the autoantibodies was one of the first aspects that was investigated. The mechanisms of autoantibody-mediated tissue/cell damage will be reviewed in Table 1.

Table 1 Mechanisms of Action of Autoantibodies

• Binding to surface membranes and subsequent destruction of the cells is a well-established pathogenic mechanism of the autoantibodies. This (cytolytic or apoptotic) cell death may involve complement-mediated, ADCC-mediated (mainly through NK or CD8+ lymphocytes) or phagocyte- mediated (opsonization) mechanisms.
• Binding to cell surface molecules, and subsequent modification of their cell biologic activity (especially when the molecule is a receptor) without cell death, is another well-established direct pathogenic mechanism of some autoantibodies. This cell activity modification may be produced by modulation, blockage, or stimulation of cell surface receptors, and usually is the main pathogenic process that explains most of the autoimmune disease.
• IC formation and tissue localization may occur in autoimmune conditions by two distinct mechanisms: (1) local formation of IC, as it happens in farmer's lung (sometimes by direct reaction with structural antigens in the local tissue); and (2) deposition of circulating ICs, as in certain glomerulonephritis (i.e., lupus nephritis).
• Some autoantibodies to intracellular proteins may bind to cell surface membranes. The two main proposed mechanisms are cross-reactions between the intracellular and the membrane antigens and translocation of the intracellular antigen to the membrane following injury or activation of the cell.
• Some evidences exists that a few autoantibodies can penetrate into living cells and others can bind to extracellular molecules.

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