This meta-analysis suggests IL1A -889 C/T polymorphism is associated with susceptibility to SLE in Europeans, and that the IL1RN*2 allele is associated with susceptibility to SLE in Europeans and Asians.
To study the relationship between clinical manifestations in systemic lupus erythematosus (SLE) with polymorphisms in suggested susceptibility genes encoding FcgammaRIIa, FcgammaRIIIa, FcgammaRIIIb, CRP and IL-1Ra.
In conclusion, our data suggest that IL-1RA gene polymorphism is not responsible for specific clinical characteristics in RA and SLE but that IL-1RN*2 is relevant in the susceptibility to RA, suggesting a protective role of IL-1RN*2 in the pathogenesis of RA.
To examine polymorphisms at IL1alpha -889(C-->T), IL1alpha +4845(C-->T), IL1beta -511(C-->T), IL1beta +3953(G-->T), and IL1Ra (86 bp VNTR) in a population based study of SLE in North Carolina and South Carolina.
Administration of cDNA encoding soluble IFN-gamma receptor (IFN-gamma R)/IgG-Fc fusion proteins, soluble TNF-alpha receptors, or IL-1 receptor antagonist (IL-1ra), protects against either lupus, various forms of arthritis, autoimmune diabetes, or other autoimmune diseases.
Synergetic effect between interleukin-1 receptor antagonist allele (IL1RN*2) and MHC class II (DR17,DQ2) in determining susceptibility to systemic lupus erythematosus.
High concentrations of IL-1Ra in the circulation and possibly in peripheral lymphoid tissues may influence immunologic and inflammatory features of SLE.