Type I interferon in the pathogenesis of systemic lupus erythematosus.

Abstract

Type I interferon (IFN) is a primary pathogenic factor in systemic lupus erythematosus (SLE). Gain-of-function genetic variants in the type I IFN pathway have been associated with risk of disease. Common polygenic as well as rare monogenic influences on type I IFN have been demonstrated, supporting a complex genetic basis for high IFN in many SLE patients. Both SLE-associated autoantibodies and high type I IFN can be observed in the pre-disease state. Patients with SLE and evidence of high type I IFN have more active disease and a greater propensity to nephritis and other severe manifestations. Despite the well-established association between type I IFN and SLE, the specific triggers of type I IFN production, the mechanisms by which IFNs help perpetuate the cycle of autoreactive cells and autoantibody production are not completely clear. This review provides an updated overview of type I IFN in SLE pathogenesis, clinical manifestations, and current therapeutic strategies targeting this pathway.

• Authors: Mariana Postal, Jessica F Vivaldo, Ruth Fernandez-Ruiz, Jacqueline L Paredes, Simone Appenzeller, Timothy B Niewold
• Journal: Current opinion in immunology (Curr Opin Immunol) Vol. 67 Pg. 87-94 (12 2020) ISSN: 1879-0372 [Electronic] England
• PMID: 33246136 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2020 Elsevier Ltd. All rights reserved.

Chemical References

• Interferon Type I

Topics

• Humans
• Interferon Type I (immunology)
• Lupus Erythematosus, Systemic (immunology, pathology)