{'fraction_non_alphanumeric': 0.06538895152198422, 'fraction_numerical': 0.05975197294250282, 'mean_word_length': 5.045996592844975, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 3, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
AB0049 REDUCED FCΓR IIB AND ENHANCED FCΓR III EXPRESSION ON MONOCYTES IN PATIENTS WITH BEHCET DISEASE

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. References [1] Aksu, K. et al. FcgammaRIIa, IIIa and IIIb gene polymorphisms in Behçet’s disease: do they have any clinical implications? Clin Exp Rheumatol. 2008;26(4 Suppl 50):S77-83. [2] Zhang, D. et al. Analysis of the association between Fc receptor family gene polymorphisms and ocular Behçet’s disease in Han Chinese. Sci Rep 2018; 19;8(1):4850. [3] Smith, KG. et al. FcgammaRIIB in autoimmunity and infection: evolutionary and therapeutic implications. Nat Rev Immunol 2010; 10(5): 328-43. [4] Su, K. et al. Expression Profile of FcγRIIb on Leukocytes and Its Dysregulation in Systemic Lupus Erythematosus. J Immunol. 2007;178(5):3272-80. [5] Li, Y. et al. Increased expression of FcgammaRI/CD64 on circulating monocytes parallels ongoing inflammation and nephritis in lupus. Arthritis Res Ther. 2009; 11(1):R6 [6] Catalán, D. et al. B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and FcgammaRIIb, which are modulated by anti-tumor necrosis factor therapy. Arthritis Res Ther. 2010;12(2):R68. Disclosure of Interests: None declared