Abstract
In rheumatic diseases several clinical entities are distinguished, many being syndromes with overlapping clinical features. For this reason, patients can evolve in the course of their disease from one diagnosis to another. In sera of many patients with rheumatic diseases highly specific autoantibodies to cellular macromolecules are detectable. Some of these autoantibodies are marker antibodies for certain diseases, e.g. antibodies reactive with double stranded DNA or the Sm antigen in systemic lupus erythematosus (SLE) [1–3]. Other examples are anti-DNA topoisomerase I (anti-Scl-70) antibodies present in sera from patients with diffuse systemic sclerosis [4], anticentromere antibodies present in sera from patients with limited systemic sclerosis [4], and anti-Jo-1 antibodies present in sera from patients suffering from polymyositis/dermatomyositis [2, 5]. Some other autoantibodies are found in more than one syndrome, e.g. anti-U1 RNP in mixed connective tissue disease (MCTD) [1, 6] and SLE [7, 8], anti-Ro60/SS-A and anti-La/SSB in Sjögren’s syndrome and SLE [9, 10], and anti-histone in both SLE and drug-induced SLE [2]. Therefore, the determination of serological autoantibodies reactive with cellular antigens located in the nucleus or the cytoplasm can be helpful in the classification of patients with rheumatic diseases [11].
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Verheijen, R., Salden, M., Van Venrooij, W.J. (1993). Protein blotting. In: Van Venrooij, W.J., Maini, R.N. (eds) Manual of Biological Markers of Disease. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5444-4_4
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