Role of complement activation in cellular activation by systemic lupus erythematosus (SLE) immune complexes (ICs)

Abstract Complement (C’) activation is a prominent feature of SLE ICs, but the mechanism by which C’ mediates cellular ICs not well understood. To investigate this question, we formed in situ healthy donor (HD) whole blood (WB) adding plasma (n=1–3;10% v/v) or HD (as control) along with apoptotic bodies (generated from RAW 264.7 cells) RNP-Sm antigen (Arotec Diagnostics, New Zealand) and without inhibitors (CI). For binding studies, WB was incubated for 45 minutes at 37°C deposition C3c human IgG (ICs) on cells examined flow cytometry. In these noted that inhibition significantly reduced B {% reduction: (97%) (97%)}, monocytes (40%) (49%)} neutrophils (69%) (70%)}. activation, 22 hours measured HLA-DR expression cytometry cytokine release (IL-8, IL-6 TNF) ELISA. Incubation made (control ICs), resulted increased (MFI control ICs: 1609 V 11096), susceptible to CI: 4975). Similarly, inflammatory also inhibited inhibition: IL-8 (75 %), (99%) TNF (99 %)}. Taken together, our results show significant C’-dependent effects activation. Additional studies are underway prevalence activating patient correlate their presence clinical disease. Wendell F. Rosse Research Award, Duke University Medical Center (SK) Scholars (GMA)