2023 Volume 83 Issue 3 Pages 181-189
Systemic lupus erythematosus （SLE） is a systemic autoimmune disease that affects multiple organs. The onset mechanism of SLE is thought to be caused by the combination of environmental and genetic factors due to disease susceptibility genes, as well as abnormalities of innate and acquired immunity. In recent years, we analyzed mitochondrial dysfunction and 27 types of immune cells extracted from the blood of patients with SLE and healthy subjects as a genetic factor and examined the expression patterns of disease-related genes. Some genes are involved in SLE and some in disease activity, and the members of both genes differ in many cells, suggesting that different pathological mechanisms are involved in SLE onset and exacerbation. Additionally, the involvement of innate immunity, such as type I interferon, has been emphasized and is attracting attention. Corticosteroids were traditionally used as SLE therapeutic agents, but in recent years, immunosuppressants, including biological agents, were rapidly developed and are being used in combination. The European College of Rheumatology recommended hydroxychloroquine administration for all patients. Mycophenolate mofetil has been proven the same as cyclophosphamide as a drug for inducing remission in lupus nephritis and is becoming the mainstream treatment. Additionally, biological agents, such as rituximab and belimumab, have been clinically applied as therapeutic agents that target the B cell system. Furthermore, the development and clinical trials of new drugs, such as voclosporin （an oral calcineurin inhibitor）, atacicept （neutralizing both B-cell-activating factor and a proliferation-inducing ligand）, iverdomide （cereblon regulator）, and Janus kinase inhibitors, are progressing, and treatment will continue to advance in the future.
