Avatar
Virgo4border

0 Following 0 Followers
1
Also associated with a more severe SLE phenotype characterized by a higher frequency of nephritis and the presence of anti-dsDNA antibodies [54]. 3.3. IFIH1 IFIH1 is an innate immune receptor located in the cytosol which senses dsRNA and promotes IRF3 and 7 phosphorylation, activating transcription of antiviral genes and type I IFN production. Based on the studies in SLE and other various autoimmu
1
With SLE and has been involved in the development of murine lupus [57, 58]. A number of studies have linked genetic variants in OPN with SLE susceptibility, clinical manifestations of SLE; and high IFN levels in SLE affected males and young-onset female lupus patients [13, 59]. OPN interacts with the MyD88 adaptor protein downstream of TLR ligation, and is an important molecule for IFN- production
1
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
1
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
1
Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
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
1
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