Pathogenesis of systemic lupus erythematosus.
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.
Mok
C C
CC
Department of Medicine and Geriatrics, Tuen Mun Hospital, Tsing Chung Koon Road, New Territories, Hong Kong. ccmok@netvigator.com
Lau
C S
CS
D000917:Antibody Formation; D001323:Autoantibodies / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D005260:Female; D005802:Genes, MHC Class II; D020022:Genetic Predisposition to Disease; D015802:HLA-DR2 Antigen / Q000235:genetics; D015803:HLA-DR3 Antigen / Q000235:genetics; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D008297:Male; D011110:Polymorphism, Genetic; D017634:Self Tolerance; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D001323:Autoantibodies; D016207:Cytokines; D015802:HLA-DR2 Antigen; D015803:HLA-DR3 Antigen