Immunopathogenesis and Therapy of Systemic Lupus Erythematosus
| Autor: | Frits H. J. Gmelig-Meyling, Ron H. W. M. Derksen, Harold Baart de la Faille, Louis Kater |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Lupus anticoagulant
Systemic lupus erythematosus Anti-nuclear antibody business.industry Lupus nephritis Autoantibody medicine.disease Antigen Antiphospholipid syndrome Immunology medicine Immunology and Allergy Pharmacology (medical) skin and connective tissue diseases business Anti-SSA/Ro autoantibodies |
| Zdroj: | Clinical Immunotherapeutics. 4:471-493 |
| ISSN: | 1172-7039 |
| DOI: | 10.1007/bf03259309 |
| Popis: | The aetiopathogenesis of systemic lupus erythematosus (SLE) is thought to comprise the combined action of hormonal influences and other factors, partly of exogenous and partly of endogenous nature, which leads to the production of autoantibodies and/or lymphoid cells, resulting in inflammatory processes. The fundamental characteristic is the occurrence in blood of autoantibodies against intranuclear cell components, usually designated as antinuclear antibodies. In addition, autoantibodies against cytoplasmically located antigens occur. Antibodies to DNA are the most prominent examples of autoantibodies, the most typical of which in SLE are antibodies to double-stranded DNA. Antibodies directed against different components of ribonucleoprotein particles include the anti-Sm, anti-SS-A (Ro) and anti-SS-B (La) antibodies. Antihistone antibodies directed against DNA-binding proteins, in particular against various histones, occur frequently in patients with drug-induced lupus. Antiphospholipid antibodies, notably lupus anticoagulant and anticardiolipin antibodies, are strongly associated with the antiphospholipid syndrome, but these antibodies can also occur in patients without features of lupus. This wide spectrum of autoantibodies implies a marked degree of chronic B lymphocyte activity. The question is whether these findings point to an intrinsic B cell aberration. There is also considerable evidence for a role of T cells in the pathogenesis of SLE. In addition, unbalanced cytokine production seems to occur. The disease also has genetic and gender aspects, and its activity may be modulated by sex hormones. Unfortunately, as the aetiology of SLE is still obscure and the pathogenetic mechanisms leading to organ disease not well understood, therapy is still limited to the use of agents with rather nonspecific anti-inflammatory properties, such as antimalarials, corticosteroids, cytotoxic drugs and apheresis. Most of these therapeutic modalities may not only benefit but also cause serious adverse effects. The eventual aim is to design immune intervention strategies, such as specific blocking peptides, by which harmful immune reactions will be eliminated leaving host defence immune reactivity intact. However, the most logical approach for immune intervention in the treatment of SLE has still to be defined. |
| Databáze: | OpenAIRE |
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