2021
DOI: 10.1016/j.cyto.2021.155633
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Abnormalities of the type I interferon signaling pathway in lupus autoimmunity

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Cited by 47 publications
(23 citation statements)
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“…Also, common polymorphisms in or near TLR7, which are related to the synthesis of interferons, seems to be involved with the development of the disease. In fact, recent evidence confirmed human SLE caused by a TLR7 gain-of-function variant ( 9 11 ).…”
Section: Sle Generalitiesmentioning
confidence: 88%
“…Also, common polymorphisms in or near TLR7, which are related to the synthesis of interferons, seems to be involved with the development of the disease. In fact, recent evidence confirmed human SLE caused by a TLR7 gain-of-function variant ( 9 11 ).…”
Section: Sle Generalitiesmentioning
confidence: 88%
“…The pathogenesis of SLE is multifactorial always with the abnormal expression of molecules that are associated with the type I IFN signaling pathway [ 14 ]. In our study, the results of GO analysis revealed that the DEGs of SCLE were primarily enriched in the response to IFN-gamma, cellular response to IFN-gamma, and type I IFN signaling pathway.…”
Section: Discussionmentioning
confidence: 99%
“…CCLE and SCLE are both common variants of CLE that may occur independently or as clinical manifestations of SLE [12,13]. Concern about the appearance of cutaneous rashes leads The pathogenesis of SLE is multifactorial always with the abnormal expression of molecules that are associated with the type I IFN signaling pathway [14]. In our study, the results of GO analysis revealed that the DEGs of SCLE were primarily enriched in the response to IFN-gamma, cellular response to IFN-gamma, and type I IFN signaling pathway.…”
Section: Discussionmentioning
confidence: 99%
“…This autoAb production results from an exacerbated IFN-I pathway that characterizes patients with systemic autoimmune diseases (SAD) [ 36 ] (Barturen et al, 2021) (Simon et al, 2021), and the presence of neutralizing anti–IFN–I autoAb lower disease activity as reported in SLE but not in RA [ 37 , 38 ]. Moreover, polymorphisms causing activation of the IFN-I pathway result in a phenotype, known as interferonopathy, which recapitulates some of the manifestations of lupus [ 39 ]. Due to the key role played by the IFN-I pathway in the physiopathology of SLE, the control of the circulating levels of IFN-I represents an interesting therapeutic option in SLE that could be exploited by targeting pDC (plasmacytoid dendritic cells) that secrete inappropriate levels of IFN-I (e.g.…”
Section: Innate Immune Response Against Sars-cov2mentioning
confidence: 99%