Background: The presence of IgA together with the myeloid IgA-receptor FcalphaRI/CD89 in the circulation of patients with IgA nephropathy (IgAN) has been suggested as a specific pathogenic factor for mesangial deposition. However, in a recent study we found these complexes also in serum samples from healthy subjects. To investigate whether these circulating complexes are specific for IgAN, the levels and characteristics of IgA-CD89 complexes were analyzed in patients with IgAN and healthy controls.
Methods: Specific ELISAs with different poly- and monoclonal antibodies and a sensitive dot-blot method were used to measure IgA-CD89 levels in serum and purified IgA samples obtained from healthy volunteers (N = 30) and patients with IgAN (N = 35). Fractionated samples of purified IgA were used to compare the size characteristics of the IgA-CD89 complexes.
Results: Almost all CD89 in serum of patients with IgAN and controls was associated with high molecular weight IgA. Quantitative analysis of IgA-CD89 complexes in purified IgA revealed no significant difference between patients with IgAN and controls. No correlation was found between levels of IgA-CD89 complexes and clinical parameters associated with progressive IgAN.
Conclusions: CD89 in the circulation is found mainly linked to high molecular weight IgA. The presence of these complexes is not specific for IgAN. Therefore, if IgA-CD89 complexes are involved in the pathogenesis of primary IgA nephropathy, additional factors are required to explain the IgA-CD89 complex-mediated renal inflammation.
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http://dx.doi.org/10.1046/j.1523-1755.2003.00756.x | DOI Listing |
PLoS One
July 2017
School of Life Sciences and Technology, Tongji University, Shanghai, China.
Although IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, its etiology remains only partly understood. It is clear that the pathogenesis of IgAN involves the formation of macromolecular IgA1 complexes and increased levels of serum IgA1 and IgA1-immune complexes(IC), due to defective IgA1 clearance. Previous studies suggest that the blood and tissue myeloid cell-expressed IgA Fc receptor (FcαR/CD89) mediates IgA-IC clearance and its dysfunction, via decreased activity or excessive levels of soluble FcαR/sCD89 induces IgAN.
View Article and Find Full Text PDFRen Fail
November 2006
Department of Laboratory Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
IgA nephropathy is the most common form of primary glomerulonephritis worldwide. The basic pathogenesis of this disease is believed to be due to the complex formation between Fc IgA, alphaRI (CD89), and transferrin receptor (CD71), leading to the damage of the glomerulus. However, studying the functional aberration in the human IgA, CD89, and CD71 complex formation in pathogenesis of IgA nephropathy is hard.
View Article and Find Full Text PDFKidney Int
March 2005
Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Primary IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis, leading to progressive renal failure in almost one third of the patients. The disease is characterized by mesangial deposits of IgA. The pathogenesis of IgAN remains incompletely understood.
View Article and Find Full Text PDFKidney Int
February 2003
Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Background: The presence of IgA together with the myeloid IgA-receptor FcalphaRI/CD89 in the circulation of patients with IgA nephropathy (IgAN) has been suggested as a specific pathogenic factor for mesangial deposition. However, in a recent study we found these complexes also in serum samples from healthy subjects. To investigate whether these circulating complexes are specific for IgAN, the levels and characteristics of IgA-CD89 complexes were analyzed in patients with IgAN and healthy controls.
View Article and Find Full Text PDFJ Immunol
February 2002
Department of Nephrology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.
The FcR for IgA CD89/FcalphaRI, is a type I receptor glycoprotein, expressed on myeloid cells, with important immune effector functions. In vitro CD89 can be released from CD89-expressing cells upon activation. Little information is available on the existence of this soluble molecule in vivo.
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