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Publication Detail
The pathogenesis of systemic lupus erythematosus
  • Publication Type:
    Journal article
  • Publication Sub Type:
  • Authors:
    Manson JJ, Isenberg DA
  • Publication date:
  • Pagination:
    343, 346
  • Journal:
  • Volume:
  • Issue:
  • Keywords:
    abnormal, ANTIGEN, Antigens, apoptosis, As, B CELL, B CELLS, B-cell, B-CELLS, behaviour, cell, cell behaviour, CELLS, COMPLEMENT, COMPLEX, COMPLEXES, COMPONENT, cytokine, deficiency, development, disease, DYSFUNCTION, environmental, etiology, EXPOSURE, function, GENE, Genes, genetic, genetics, heterogeneous, IM, immune, immune regulation, immunology, Infection, LA, LIGHT, Lupus, Lupus Erythematosus, Systemic, May, MECHANISM, multiple, novel, nuclear, NUCLEAR ANTIGEN, NUMBER, PATHOGENESIS, play, regulation, Review, SLE, SUSCEPTIBILITY, SYSTEMIC, SYSTEMIC LUPUS ERYTHEMATOSUS, SYSTEMIC-LUPUS-ERYTHEMATOSUS, T cell, T-CELL, target, technique, techniques, understanding, viral
  • Notes:
    DA - 20040210 IS - 0300-2977 LA - eng PT - Journal Article PT - Review PT - Review, Tutorial SB - IM
SLE is a complex, heterogeneous disease, the precise pathogenesis of which remains something of a mystery. In recent years our understanding has been advanced by the development of novel genetic and immunological techniques. Susceptibility to SLE has a genetic component and multiple putative genes are being investigated. The genes involved are likely to play a part in immune regulation. Central to the immune dysfunction seen in SLE is the presence of autoreactive B cells, which predominantly target nuclear antigens. In addition to evidence of aberrant B and T cell behaviour, lupus is associated with complement deficiencies, and abnormal cytokine function. A number of environmental triggers exist, and likely candidates include viral infection and exposure to UV light. Finally, evidence is accumulating that implicates apoptosis as a mechanism by which disease may be provoked and propagated
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