The role of pro-inflammatory cytokines in systemic lupus erythematosus (SLE) 
remains somewhat controversial. Several studies have shown increased production 
of TNF alpha and IL-6 in patients with SLE. Increased production of IL-6, TNF 
alpha, and IL-1 soluble receptors have also been reported. This finding is 
provocative because the soluble receptors have the capacity to act as 
antagonists. Several other inflammatory disorders are also associated with 
increased production of soluble TNF alpha receptors suggesting that this may be 
a general compensatory mechanism designed to down-regulate inflammation. The 
recent identification of an SLE disease susceptibility locus near the TNFR2 
locus (TNFR p75) suggested the hypothesis that genetically driven differences in 
soluble TNFR2 production could play a role in the genetic susceptibility to SLE. 
We therefore characterized the frequency of a genetic polymorphism in the 3' 
untranslated region of the TNFR2 gene in Caucasoid SLE patients and 
geographically matched controls. No difference in the gene frequency of the two 
base-pair polymorphism in SLE patients compared to controls was found, nor was 
there any association with any particular clinical phenotype.