SAT0003 Quantitative Monocyte CD64 (MCD64) Expression is Useful Biomarker for Disease Activity in Systemic Lupus Erythematosus (SLE) Patients

Background Interferon (IFN)-α has been largely implicated in the ethiopathogenesis of SLE. The activation of IFN-α might be important in the prognosis and activity assessment of the disease. CD64 (FcγRI) is upregulated on monocytes as a response to IFN-I 1 . Flow cytometry analysis of mCD64 expression (Mean Fluorescence Intensity) is a convenient and rapid approach for estimating IFN-α levels in SLE patients. Additionally, macrophage colony-stimulating factor (M-CSF), which is involved in the differentiation of monocyte/macrophage, affects CD64 expression on monocyte 2 has been reported to increase in levels in SLE patients, 3 and is also involved in SLE disease activity 4 . mCD64 can be the quantified easily and the measurement is consistent among the respective facilities. However, the quantitative mCD64 of SLE patients has not been reported. Objectives We investigated the levels of mCD64 by quantitative flow cytometry to assess the usefulness of it as a SLE disease activity biomarker. Methods 30 SLE patients (10 active SLE, 20 inactive SLE) and 20 healthy controls (HC) were in this study. SLE disease activity was evaluated using by SLE-Disease Activity Index (SLEDAI) score. mCD64, SLE activity biomarkers (anti-DNA antibody and complement titer (CH50)), IFN-α and M-CSF were measured in SLE patients. mCD64 was measured by a quantitative flow cytometry using fluorescene microbeads. INF-α and M-CSF levels were measured using an enzyme-linked immunoabsorbent assay (ELISA). Correlational analysis between levels of mCD64, SLEDAI, SLE activity biomarkers, INF-α and M-CSF in each group were evaluated. Results Disease activity markers are shown Table 1. The variables with significant difference between active SLE and inactive SLE were SLEDAI (p Conclusions This study suggests that quantitative CD64 molecules expressed on monocytes can be a useful disease activity biomarker in SLE patients. References Li, Y. et al. Arthritis Research & Therapy 2010, 12:R90 Ji XH et al. Acta Pharmacol Sin. 2004; 25(10): 1361-5 Yang PT et al. Ann Rheum Dis. 2008, 67(3): 429-30 Tsuji S. et al. The Journal of Tokyo Medical University vol.70, No.1: 151-8 Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2824