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Virgo4border

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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
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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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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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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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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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D to other immune system functions such as B- and T- cell signaling, clearance of dead cellular debris, and cytokine signaling make up a large portion of the genetic loci associated with SLE. In this review, we will discuss polygenic and monogenic influences on type I IFN, as well as the functional significance of some of the other SLE-associated polymorphisms located in immune system genes. These
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E, there is approximately ten-fold higher risk for SLE in monozygotic twins than in dizygotic twins [9, 10], while first degree relatives of patients with SLE have a 20-fold increased risk of developing SLE as compared with the healthy population [3, 11]. Within the families with multiple affected members, the SLE occurrence does not usually follow a classical Mendelian inheritance pattern. In the