The interferon-α signature of systemic lupus erythematosus Review uri icon

Overview

MeSH Major

  • Interferon Type I
  • Interferon-alpha
  • Lupus Erythematosus, Systemic

abstract

  • 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.

publication date

  • August 2010

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3658279

Digital Object Identifier (DOI)

  • 10.1177/0961203310371161

PubMed ID

  • 20693194

Additional Document Info

start page

  • 1012

end page

  • 9

volume

  • 19

number

  • 9