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J Clin Pathol 2003;56:481-490 doi:10.1136/jcp.56.7.481
  • Review

Pathogenesis of systemic lupus erythematosus

  1. C C Mok1,
  2. C S Lau2
  1. 1Department of Medicine and Geriatrics, Tuen Mun Hospital, Tsing Chung Koon Road, New Territories, Hong Kong
  2. 2Department of Medicine, Queen Mary Hospital, Hong Kong, SAR, China
  1. Correspondence to:
 Dr C C Mok, Department of Medicine and Geriatrics, Tuen Mun Hospital, Tsing Chung Koon Road, New Territories, Hong Kong; 
 ccmok{at}netvigator.com
  • Accepted 12 February 2003

Abstract

The exact patho-aetiology of systemic lupus erythematosus (SLE) remains elusive. An extremely complicated and multifactorial interaction among various genetic and environmental factors is probably involved. Multiple genes contribute to disease susceptibility. The interaction of sex, hormonal milieu, and the hypothalamo–pituitary–adrenal axis modifies this susceptibility and the clinical expression of the disease. Defective immune regulatory mechanisms, such as the clearance of apoptotic cells and immune complexes, are important contributors to the development of SLE. The loss of immune tolerance, increased antigenic load, excess T cell help, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2 immune responses leads to B cell hyperactivity and the production of pathogenic autoantibodies. Finally, certain environmental factors are probably required to trigger the disease.

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