Abstract: 【Abstract】Objective Increasing evidences indicated that the initial pathogenic factor for IgA nephropathy (IgAN) was the abnormal IgA molecule. IgA molecules are produced from peripheral B-lymphocytes. However, the limited availability of B-lymphocytes greatly hindered the studies in depth on mechanisms in IgAN. Recently, EBV (Epstein-Barr virus)-immortalized B-cells were reported to maintain the characteristic of secreting aberrant glycosylated IgA1 molecules, and were regarded as a useful cell model for studies on mechanisms leading to aberrant IgA1 glycosylation in IgAN. A recent genome-wide association study in IgAN identified a proliferation-inducing ligand (APRIL) as one of IgAN susceptible genes. The objective of this study was to investigate the feasibility of EBV-immortalized B-cells for study of APRIL in IgAN. Methods We established three EBV-immortalized B-cell lines from three individuals with distinct diseases. After treated with different doses of APRIL (1.56-200 ng/ml) for 48 hours, conditioned media from these EBV-immortalized B-cells were collected for detection of IgA level by ELISA. Meanwhile, primary B-lymphocytes isolated from peripheral blood of a healthy control were treated with 25 ng/ml APRIL, and IgA in the conditioned media were also detected. Results APRIL significantly promoted the secretion of IgA in primary B-lymphocytes (294.3±35.7 ng/ml vs. 368.2±36.2 ng/ml, P=0.043), but not in EBV-immortalized B-cells (P value >0.05 was observed in APRIL of 1.56-200 ng/ml). Conclusion Our study identified the different effect on IgA secretion induced by APRIL between primary B-lymphocytes and EBV-immortalized B-cells, suggesting that EBV-immortalized B-cells may not be suitable for the study of APRIL on IgA in IgAN.

Key words: IgA nephropathy, Epstein–Barr virus, a proliferation-inducing ligand, B lymphocyte