Decreased expression of FcγRII in active Graves' disease patients. Issue 6 (29th April 2019)

• Record Type: Journal Article
• Authors: Lu, Xixuan; Peng, Shiqiao; Wang, Xinyi; Shan, Zhongyan; Teng, Weiping
• Is Part Of: Journal of clinical laboratory analysis. Volume 33:Issue 6(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-04-29
• Subjects: autoimmunity -- CD32B -- FcγR -- FcγRII -- Graves' disease; Diagnosis, Laboratory -- Periodicals; Medical laboratory technology -- Periodicals; 616
• DOI: 10.1002/jcla.22904
• Languages: English
• ISSNs: 0887-8013

Abstract

Abstract: Background: Graves' disease (GD) is a common autoimmune disease characterized by genetic and environmental factors. Fcγ receptors (FcγRs) are involved in several autoimmune disorders through recognizing immunoglobulin (Ig) G antibodies and mediating immune response. The study on the expression of FcγRs in GD patients is scarce. The purpose of this study was to evaluate the expression of three different types of FcγRs in patients with active and remissive GD. Methods: Blood samples of patients and healthy subjects were collected to analyze the percentage of FcγRI (CD64), FcγRII (CD32), and FcγRIII (CD16) on peripheral blood mononuclear cells (PBMCs) and monocytes by flow cytometry and Western blotting. CD32 isotypes were also examined in cases and controls by real‐time PCR. Results: The cell percentages expressed CD32 and protein expressions of CD32 on PBMCs, and monocytes from patients with active GD were significantly reduced compared to controls and patients with remissive GD. In particular, the expression of CD32B on PBMC was also decreased in active GD patients. However, the cell percentages expressed CD16 and CD64 from PBMCs and monocytes were comparable between three groups. Besides, the percentages of CD14 + CD32 + cells were negatively correlated with TRAb titers in active GD patients ( r = −0.5825, P ＜ 0.001). Conclusion: These results suggested that CD32 may act as a novel marker for active GDs. The expression of monocytic CD32, in particular CD32B, in GD patients might play a crucial role in maintaining FcγRs function and be a therapeutic target in GD patients.