论文部分内容阅读
Aim Immunoglobulin D (IgD) is a surface immunoglobulin that is expressed as either membrane IgD(mIgD) or secreted IgD (sIgD).Researchers have shown that sIgD is often elevated in patients with autoimmune diseases.The possible roles of sIgD on the function of peripheral blood mononuclear cells (PBMCs) in rheumatoid arthritis (RA) are still unclear and few studies have been performed.The objective of this study was to investigate the abnormal level of immunoglobulin D (IgD) and the effects of it by binding its receptor (IgDR) on peripheral blood mononuclear cells (PBMCs) in rheumatoid arthritis (RA).Methods Blood samples were obtained from 54RA patients and 42 healthy controls.The levels of sIgD, human soluble receptor activator of nuclear factorκB ligand (sRANKL), anticyclic citrullinated peptide (antiCCP), Creactive protein (CRP) were determined in serum samples by ELISA.Rheumatoid factor (RF) was detected by quantitative nephelometry.Erythrocytes sedimentation rate (ESR) was tested by Westergren method.IgDR and mlgD were detected by using flow cytometry.After PBMCs were cultured and treated with different concentrations of human IgD.PBMCs proliferation were measured by CCK8, inflammatory cytokine production were assessed by inflammation antibody array, T/Bcell subsets and IgDR expression were tested by flow cytometry.Results A significantly higher level of sIgD, mlgD and IgDR were detected in RA patients compared with healthy controls.The concentrations of sIgD were positively correlated with sRANKL, rheumatoid factor and Creactive protein in RA patients.Strikingly, IgD could enhance the proliferation of PBMCs and induce IL1 α, IL1β, TNFα, IL6 and production from PBMCs.Moreover, the percentage of activated T cell subsets (CD4 + CD69 + , CD4 + CD154 +) and activated B cell subsets (CD19 + CD23 + , CD19 +CD21 + , CD19 + IgD + and CD19CD138 +) were increased by IgD.The percentage of unactivated T cell subset(CD4 + CD62L +) and immature B cell subset (CD19 + IgM + IgD) were decreased by IgD in PBMCs.Furthermore, the expressions of IgDR on T and B cells were significantly increased by treatment with IgD.Conclusion IgD enhanced the activation of PBMCs through stimulation of IgDR, which may contribute to RA pathogenesis.IgD represents a potentially novel immunotherapeutic target for the management of RA.