Abstract

Background: Behcet’s disease (BD) is a systemic inflammatory disease without clear pathogenesis. Previous studies have shown the association between FcγR gene polymorphisms and BD1-2. FcγRs, the receptor of IgG, has both activatory and inhibitory subtypes, and the imbalance of them on immunocytes has been illustrated to have significant pathogenetic roles in many autoimmune diseases3-6. Objectives: This study was aimed to investigate the potential abnormal expression of FcγRs in BD patients Methods: We recruited 27 newly-onset treatment-naive BD patients (according to 2014 International Criteria for BD) and 23 gender-and age-matched healthy controls (HC). Flow cytometry was used for detecting the expression of the inhibiting receptor (FcγRIIB) and activating receptors (FcγRI and FcγRIII) on the neutrophils, monocytes, B cells, natural killer cells, dendritic cells, and T cell from the whole blood of BD and HC. The correlation between the expression of FcγR and disease activity index of BD was evaluated. Results: BD patients had increased numbers of monocytes (60.14±3.387% vs 47.56±4.923%, p=0.0365) compared with HC. FcγRIIB expression on monocytes, rather than other immunocytes (p>0.05), was significantly lower in BD patients (4.87±0.61% vs 7.67±1.10%, p=0.0199). FcγRIIB expression on monocytes was negatively correlated to ESR (r=-0.576, p=0.031) and CRP (r=-0.539, p=0.047), positively correlated to serum IgA (r=0.785, p=0.001) and uncorrelated to serum IgG, IgM and PLT (p>0.05). FcγRIII expression on monocytes was higher in BD patients (19.61±3.046% vs 9.349±1.107%, p=0.0091). FcγRIII expression on monocytes was positively correlated to ESR (r=0.2551, p=0.0274) and CRP (r=0.2354, p=0.0352), and uncorrelated to serum IgG, IgM, IgA and PLT (p>0.05). Furthermore, FcγRIIB expressions of monocyte were comparable between BD patients in active disease or remission, while FcγRIII expression was significantly decreased (p=0.0158) after 3-month of treatment. Conclusion: Our research demonstrated, for the first time, that the decreased expression of inhibitory receptor FcγRIIB and increased expression of activatory receptor FcγRIII on monocytes in BD. Furthermore, the abnormal expression was correlated with disease activity. These findings suggested that FcγRs ratio imbalance might play a role in the pathogenetic role of BD.

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