期刊
CURRENT OPINION IN IMMUNOLOGY
卷 67, 期 -, 页码 87-94出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2020.10.014
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资金
- Fundacao de Amparo a Pesquisa do Estado Sao Paulo-Brasil [FAPESP 2008/02917-0, 2016/23269-3]
- Conselho Nacional Pesquisa Desenvolvimento-Brasil CNPq [300447/2009-4, 471343/2011-0, 302205/2012-8, 473328/2013-5, 157534/2015-4]
- Coordenacao de Aperfeicaoamento de Pessoal de Nivel Superior -Brasil (CAPES) [001]
- Niewold TB: Colton Center for Autoimmunity, NIH [AR060861, AR057781, AR065964, AI071651]
- Lupus Research Foundation
- Lupus Research Alliance
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [16/23269-3, 08/02917-0] Funding Source: FAPESP
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.
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