Anti-CD11b (Integrin alpha-M) monoclonal antibody, clone SN300

BackgroundEvidence has indicated that peroxisome-proliferator activated receptor- (PPAR-) agonists could be used in the prevention and treatment of murine systemic lupus erythematosus (SLE). However, to our knowledge, just one previous study has focused on the association between PPAR- polymorphisms and SLE in humans. AimTo investigate the association between PPAR- polymorphisms and SLE in a Chinese population and on additional gene-gene interaction between multiple single nucleotide polymorphisms (SNPs) in PPAR-. MethodsThree SNPs of PPAR- were selected for genotyping in this case-control study: rs1805192, rs10865710 and rs709158. Logistic regression was used to examine the association between the three SNPs and SLE, and the odds ratio (OR) and 95% CI were calculated. Generalized multifactor dimensionality reduction (GMDR) was used to investigate additional interaction. ResultsAll genotypes were distributed according to Hardy-Weinberg equilibrium. Logistic regression analysis showed a significant association between genotypes of rs1805192 variants and decreased SLE risk, after adjustment for sex, age, smoking, high-fat diet, low-fibre diet, alcohol status, body mass index and waist circumference. Participants with Ala allesles had a lower SLE risk than those homozygous for the wild-type allele (OR=0.78; 95% CI 0.69-0.92). GMDR analysis indicated that there was a significant two-locus model (P=0.001) involving rs1805192 and rs10865710, indicating a potential gene-gene interaction between them. Overall, the two-locus models had a cross-validation consistency of 10 out of 10 and a testing accuracy of 60.72%. ConclusionsThere was a significant association between PPAR- rs1805192 genotypes and decreased SLE risk, and a potential gene-gene interaction between rs1805192 and rs10865710.

Background and objectivesSystemic lupus erythematosus (SLE) is a chronic autoimmune disease with unknown etiology. Genetic and environmental factors play important roles in the pathogenesis of SLE. The primary objective of this study was to investigate the possible association of eNOS gene intron 4b/a, Glu298Asp and T-786C polymorphisms with SLE in southeast Iran populations. Patients and methodsThis was a case-control study comparing eNOS polymorphisms in 106 SLE patients and 196 age- and sex-matched healthy controls. The 4b/a, Glu298Asp and T-786C polymorphisms were analyzed using polymerase chain reaction and restriction fragment length polymorphism. ResultsOur findings indicated that the 4b/a polymorphism was associated with SLE, and the risk of SLE was 3.5- and 1.75-fold higher in patients with aa and ba genotypes than in patients with bb genotype. No association was observed between Glu298Asp and T-786C polymorphisms and SLE. There were no differences in eNOS gene polymorphisms between the Balouch and Fars population. ConclusionStatistically significant differences were observed in genotypes and allele frequencies of 4b/a polymorphism between patients with SLE and healthy controls in southeast Iran.