Systemic Lupus Erythematosus

Pathophysiology

Systemic lupus erythematosus (SLE) is a multisystem, chronic, autoimmune disorder in which different body systems (joints, skin, kidneys, brain, heart, and lungs) are affected by inflammation.1,2 SLE is characterized by activation of autoreactive lymphocytes, production of autoantibodies, and complement activation.3 The pathogenesis of SLE depends on various genetic and environmental factors, including the following: the contribution of major histocompatibility complex class I and II genes; a dysregulated hypothalamic-pituitary-adrenal axis; increased activity of estrogen in the context of reduced androgen activity; abnormal activation of T and B cells and the resulting production of pathogenic autoantibodies; and environmental exposure to chemicals and drugs, ultraviolet light, dietary factors, viruses, and environmental estrogen.4,5 Although the specific genetic causes of SLE have not been fully elucidated, polymorphisms in genes encoding Ikaros and Aiolos have been associated with an increased risk of developing SLE.6 Ikaros and Aiolos are key members of the Ikaros family of zinc-finger transcription factors that promote B-cell development and regulate responses of T-cells and plasmacytoid dendritic cells.6,7

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The safety and efficacy of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.

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Clinical trial information is sourced from ClinicalTrials.gov. Information is updated manually as clinical trials are published. The efficacy and safety of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.

References

  1. American College of Rheumatology. https://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Lupus
  2. Lupus Foundation of America. https://www.lupus.org/resources/lupus-facts-and-statistics
  3. Crampton SP, et al. Dis Model Mech. 2014;7:1033-1046. PMID:25147296
  4. Mok CC, Lau CS. J Clin Pathol. 2003;56:481-490. PMID:12835292
  5. Choi J, et al. Curr Opin Immunol. 2012;24:651-657. PMID:23131610
  6. Nakayama Y, et al. J Immunol. 2017;199:2388-2407. PMID:28848067
  7. Allman D, et al. Blood. 2006;108:4025-4034. PMID:16912230