Background Clinical decision-making in the management of fever is difficult when distinguishing infection and high disease activity in SLE. CD64 (FcγRI) is upregulated on monocytes as a response to interferon (IFN)-α in SLE1. In infection, upregulation of CD64 expression on neutrophils occurs with IFN-γ, granulocyte colony stimulating factor, or lipopolysaccharide. CD64 on neutrophils is known to be a sensitive and specific marker for detection of infection in rheumatoid arthritis patients (using a cutoff value of 2000 molecules per cell)2.
Objectives We examined the utility of quantitative CD64 molecules expressed on monocytes and neutrophils, and calculated mCD64/nCD64 ratio as a marker for distinction between infection and disease activity in SLE.
Methods In this study, 12 SLE patients with infections (iSLE), 10 SLE patients with high disease activity, (aSLE) (SLEDAI 12.1±7) and 20 healthy controls (HC) were enrolled. The expression level of CD64 per monocyte and neutrophil quantitatively were measured by flow cytometry, and the mCD64/nCD64 ratio were calculated. Comparisons of levels within each group were analyzed, and levels of respective measurements at both pre- and post-treatment were analyzed.
Results Results of mCD64, nCD64 and m/nCD64 ratio are presented in Table1. The nCD64 value of iSLE and aSLE was 2000 molecules/cell or more together. There was no difference in mCD64 of iSLE and aSLE. m/nCD64 ratio was significantly lower among iSLE than in those without infection, aSLE, or healthy controls (p<0.001). After each treatment, the value of mCD64 and nCD64 were significantly decreased in iSLE and aSLE. But there was no change in mCD64/nCD64 ratio in aSLE, on the other hand it was increased in iSLE (p<0.01).
Conclusions A cutoff value of 2000 molecules per cell on neutrophils did not clearly distinguish infection from exacerbation in SLE. However, our results suggest that calculating m/n CD64 ratio can be useful to distinguish infection or disease activity in SLE. Moreover, combined mCD64 and nCD64 could help to guide therapeutic decision in SLE.
Li, Y. et al. Arthritis Research & Therapy 2010, 12:R90.
Matsui, T. et al. The Journal of Rheumatology 2006; 33: 2416-24.
Disclosure of Interest None declared