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Ect interaction with MyD88, but it does appear to play a role in the TLR pathway as dendritic cells lacking IRF8 do not produce inflammatory cytokines in response to TLR9 ligand [48]. IRF8 deficiency in humans results in an immunodeficiency characterized by the loss of monocytes and dendritic cells, indicating its role in monocyte and dendritic cell development [49]. Genetic variants in the IRF8 g
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Of evidence indicate that abnormalities in the apoptosis (programmed cell death) contribute to the development of SLE, as the elimination of autoreactive T or B cells is impaired in this disease [67]. In addition, it appears that increased lymphocyte apoptosis and delayed clearance of phagocyte-mediated apoptotic cells as evident in SLE patients could contribute to B-cell hyperactivity and subsequ
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Nducing IFN- and IFNinduced genes downstream of Toll-like receptor (TLR) activation. Additionally they play prominent role in cytokine secretion, cellular apoptosis, immune cell development, tumor suppression, and cell activation and differentiation [38, 39]. Interestingly, genetic variations in three of the nine IRFs (IRF5, IRF7, and IRF8) have been linked to SLE susceptibility, supporting a key
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On IRF5 in human SLE cohorts have shown that the risk variant predisposes to greater serum IFN-, supporting the idea that the risk haplotype is a gain-offunction variant [22]. The same risk variant has been associated with autoantibody formation in SLE patients and in healthy individuals, and most of the risk of SLE related to IRF5 genotype is found within the autoantibody positive, high IFN group
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Important role in downstream responses to type I IFN and other cytokines. Functionally, activation and phosphorylation of STAT4 is induced by IL-12, IL-23, and IFN- which then promotes Th1 as well as Th17 responses [53]. Both candidate gene association studies and multiple GWAS studies using populations from European or Asian ancestry have demonstrated a robust association between SLE and STAT4 [1
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Nducing IFN- and IFNinduced genes downstream of Toll-like receptor (TLR) activation. Additionally they play prominent role in cytokine secretion, cellular apoptosis, immune cell development, tumor suppression, and cell activation and differentiation [38, 39]. Interestingly, genetic variations in three of the nine IRFs (IRF5, IRF7, and IRF8) have been linked to SLE susceptibility, supporting a key
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Al blood cells in anti-dsDNA positive SLE patients, and was associated with the production of anti-dsDNA antibodies [55]. Recently, a large-scale multiancestral admixture mapping genetic screen revealed three independently associated variantsJ Autoimmun. Author manuscript; available in PMC 2016 November 01.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptGhodke-Puranik and Ni
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T human IFN- is used as a treatment for MS. A study investigating whether IRF8 alleles were associated with type I IFN levels or serologic profiles in SLE and MS revealed that MS-associated allele downstream of IRF8 (rs17445836G) was associated with decreased activity of the type I IFN pathway in these two different autoimmune diseases and was associated with anti-dsDNA antibodies and increased IR