Key autoantigens in SLE

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Abstract
Murine and human systemic lupus erythematosus (SLE, lupus) is characterized by the appearance of autoantibodies directed to nuclear and cell membrane phospholipid components. Some functionally related nucleic acid-containing macromolecules such as chromatin or ribonucleoprotein particles are specifically targeted both by autoantibodies and T cells involved in lupus pathogenesis. In the last decade, the identification of target structures has strongly improved diagnostic tools. Furthermore, characterization of autoantigens has provided insight into pathogenic mechanisms to understand why these autoantigens are recognized in SLE. However, the recognition of autoantigens and a stable immune response towards these specificities requires the coincidence of several events (such as environmental triggers in the external world) plus abnormalities in genetically susceptible organisms that modify normal immune responses. Furthermore, the persistence of the autoantibody response in lupus long after the initial trigger suggests that endogenous autoantigens (from the internal world) are important in sustaining the ongoing immune response. Once the critical threshold is breached, there is a failure of the immune system to down-regulate normal immune responses which thus become abnormal and persistently autoreactive [1]. The importance of different events and genes that initiate and/or maintain the autoimmune response may vary from patient to patient, all resulting in the characteristic autoimmune features and pathology of this systemic autoimmune disease.

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