Results Expression of candidate biomarkers in the SLE cohort To determine whether previously reported biomarkers were elevated in our SLE patient cohort, we measured the biomarker expression levels in HD, active chronic myelocytic leukemia SLE, and inactive SLE patient visits. The SLE cohort was segregated by SLEDAI into active SLE and inactive SLE. Inhibitors,Modulators,Libraries The level of IFN I was estimated by quantifying the ex pression of IFN inducible genes. The IFN score, STAT1, ADAR, CCL2, and CXCL10 levels were significantly ele vated at both active and inactive SLE patient visits com pared to HD, establishing and confirming that these biomarkers were aberrantly overexpressed in our SLE patients. To explore if these biomarkers were capable of distinguishing disease activity status, active and inactive patient visits were compared to one another.
No significant difference was observed between active and inactive SLE patient visits for IFN score, ADAR, and CXCL10, but STAT1 and CCL2 were significantly elevated in active SLE com pared to inactive SLE patient visits. TNF, which is not generally involved in the pathogenesis of SLE, was used as a negative control. As Inhibitors,Modulators,Libraries expected, TNF was Inhibitors,Modulators,Libraries not significantly different among the three groups. Similarly miR 146a did not display any significant difference among active SLE, inactive SLE, and HD. To validate this, we determined the levels of the primary transcript of miR 146a which also did not demonstrate any significant difference among active SLE, inactive SLE, and HD. With the exception of miR 146a, these results are consistent with reports on SLE patients with elevated IFN score compared to HD as well as upregulated levels of IFN signature genes and chemokines.
The clinical and expression data were correlated with anti dsDNA autoantibody level, which is an indicator for patients disease activity in certain patients. De creases in C3 and C4 levels correlated with SLE activity and renal damage as well as increased levels of anti dsDNA antibodies. Anti dsDNA autoantibody levels have also been used for sub Inhibitors,Modulators,Libraries classification of SLE patients. SLE patient visits and HD were segregated into anti dsDNA and anti dsDNA. Patient visits that were anti dsDNA displayed higher SLEDAI and decreased C3 and C4 levels. The results for the remaining biomarkers closely resembled those from active versus inactive SLEDAI results. The influence of race in anti dsDNA, IFN score, STAT1, CCL2, and CXCL10 were also examined.
African Americans and European Americans Inhibitors,Modulators,Libraries contributed to 83. 3% of the visits, followed by Latin Americans and Asian Americans for 15%, selleck inhibitor and interracial Americans for less than 2% of patient visits. Due to the small sample size, IrA were excluded in all subsequent analyses. In general, results show that higher levels of anti dsDNA, IFN score, STAT1, CCL2, and CXCL10 were observed in all race groups analyzed.