The interferon-α signature of systemic lupus erythematosus

Lupus - Tập 19 Số 9 - Trang 1012-1019 - 2010
Gerlinde Obermoser1, Virginia Pascual2
1Baylor Institute for Immunology Research, Dallas, TX, USA, , Department of Dermatology, University Hospital Innsbruck, Innsbruck Medical University, Austria
2Baylor Institute for Immunology research, Dallas, TX, USA

Tóm tắt

Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease’s unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention. Lupus (2010) 19, 1012—1019.

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Lupus

Tập 19 Số 9

1012-1019

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