Background Polymorphisms in the Fcγ receptor (FcγRI, FcγRIIa, and FcγRIIb and FcγRIIIa genes) have been associated with an increased susceptibility to autoimmune diseases including SLE and up-regulation of these may vary with disease activity and infection. There is a paucity of data on FcγR expression pattern in pediatric subjects with SLE.
Objectives To assess the expression of CD 64 (FcγRI), CD32b (FcγRIIb) and CD16 (FcγRIII) on B lymphocytes, neutrophils and monocytes in children with pediatric-onset SLE (pSLE) and their correlation with disease activity as estimated by the SLEDAI score.
Methods A cross - sectional descriptive study was conducted at PGIMER, Chandigarh, India. Children aged between 0 and 15 years fulfilling American College of Rheumatology classification criteria (1997) for SLE were enrolled. The study population was divided into active and inactive group using SLEDAI score. Controls were age and sex matched.
Blood samples of cases and controls were assessed for CD 64, CD32b, and CD16 expression on B lymphocytes, neutrophils and monocytes by flow cytometry using standard techniques. Median fluorescence intensity (MFI) and percentage of cells expression were calculated using the FACS DIVA software and Kaluza software.
Results Thirty one children with SLE (14 in active group) and 13 controls were analyzed. The median values of percentage expression of CD 64 on lymphocyte and monocytes and MFI of CD16 on neutrophils in cases and control are tabulated.
Statistically significant difference (p<0.05) in expression of CD64 on lymphocytes, MFI of CD16 on neutrophils was noted in cases as compared to controls, while there was no difference between active and inactive cases. No difference was noted in expression of CD64 on monocytes between cases and controls.CD20 was reduced in cases probably secondary to therapy.
Conclusions The percentage expression of CD 64 expression in lymphocytes and MFI of CD 16 expression in neutrophils were increased in patients of pSLE but no significant association was obtained with disease activity. There is paucity of data in pSLE and thus further studies are warranted to substantiate our finding. No correlation of CD16 and CD32b expression with disease activity was noted in our cohort, probably due to the small sample size.
Disclosure of Interest None declared
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