Pathogenesis of systemic lupus erythematosus
By C. Mok, C. S. Lau. Journal of Clinical Pathology, 2003
1,111 citations recorded by the source corpus.
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.
Subfields: Immunology, Radiology, Nuclear Medicine and Imaging, Rheumatology
View Paper: https://www.semanticscholar.org/paper/f46cecc97be96c50ece208de9b5f5df382ecf4e5
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Citations in the corpus
- Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9. (2005, background): “Introduction Systemic lupus erythematosus (SLE), the second most common autoimmune disorder, after rheumatoid arthritis and the prototypic immune complex (IC) disease, is characterized by autoantibody production and IC formation, which results in immunologically mediated tissue injury (1, 2).”
- Foxp3 reprograms T cell metabolism to function in low glucose high lactate environments (2017, background): “Tissue injury risks exposure of antigens such as histones and double-stranded DNA that exceed the clearance capacity of phagocytic cells, which may predispose to autoimmune disease (Mok and Lau, 2003).”
- Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE (2007, background): “The blue line is “Ins(1,3,4,5)P4 (300 μM)” and the green line is “Ins(1,4,5,6)P4 (300 μM).”