Abstract
BackgroundGraves' 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.MethodsBlood 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.ResultsThe 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).ConclusionThese 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.
Highlights
Graves' disease is a common autoimmune disorder that has a multi‐ faced etiology involving genetic and environmental factors and is featured by the presence of thyroid stimulating hormone receptor (TSHR)‐stimulating antibodies (TSAbs) that can promote the func‐ tion of thyroid follicular cells (TFCs) and stimulate thyroid growth, and lead to an overproduction of thyroid hormones (TH).[1]
We reported for the first time that decreased cell percentages ex‐ pressed FcγRII (CD32) as well as decreased protein levels of FcγRII from peripheral blood mononuclear cells (PBMCs) and monocytes have been found in patients with active
Our results showed that the expression of CD32B on PBMCs was reduced in active Graves' disease (GD) patients, which was consis‐ tent with other studies on CD32B expression in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).[13,23]
Summary
Graves' disease is a common autoimmune disorder that has a multi‐ faced etiology involving genetic and environmental factors and is featured by the presence of thyroid stimulating hormone receptor (TSHR)‐stimulating antibodies (TSAbs) that can promote the func‐ tion of thyroid follicular cells (TFCs) and stimulate thyroid growth, and lead to an overproduction of thyroid hormones (TH).[1]. Activation of activatory FcγRs causes immune responses such as antibody‐dependent cell‐mediated cyto‐ toxicity (ADCC) and antibody‐dependent cell‐mediated phagocytosis (ADCP), while crosslinking of the inhibitory FcγRIIB such as colliga‐ tion of FcγRIIB with BCR can negatively regulate the activation and proliferation of B cell and inhibit IgG production.[6]. These three types of FcγRs are all expressed on human monocytes. CD16 is a re‐ ceptor with average affinity for IgG, which is expressed on approxi‐ mately 10% of monocytes.[8] Of these FcγRs, CD16, CD32A, and CD64 are activatory Fcγ receptors with intracytoplasmic tyrosine‐based activatory motifs that induce monocytes initiation under receptor polymerization. We analyzed the correlation between the expression levels of FcγRs with autoantibodies
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