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Research Article Free access | 10.1172/JCI114269

Humoral immune response to influenza vaccination in patients with primary immunoglobulin A nephropathy. An analysis of isotype distribution and size of the influenza-specific antibodies.

A W van den Wall Bake, W E Beyer, J H Evers-Schouten, J Hermans, M R Daha, N Masurel, and L A van Es

Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Department of Nephrology, University Hospital, Leiden, The Netherlands.

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Published October 1, 1989 - More info

Published in Volume 84, Issue 4 on October 1, 1989
J Clin Invest. 1989;84(4):1070–1075. https://doi.org/10.1172/JCI114269.
© 1989 The American Society for Clinical Investigation
Published October 1, 1989 - Version history
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Abstract

Primary IgA nephropathy (IgAN) is characterized by mesangial deposits of IgA1, increased serum IgA1 levels, and circulating immune complexes containing predominantly IgA1. It has previously been found that patients with IgAN have a higher than normal IgA response to vaccination, but the IgA subclasses have not been studied. To investigate whether the IgA hyperresponsiveness is limited to the subclass IgA1, which is involved in the pathogenesis of IgAN, we compared the immune responses of 18 patients with 22 healthy controls after intramuscular vaccination with inactivated influenza virus. Antibody titers were significantly higher (P less than 0.0001) for the IgA1 subclass in patients versus controls, but not for the other isotypes. A substantial portion of the IgA and IgA1 antiinfluenza immune response comprised polymers in both patients and controls. There was no preferential response of polymers in patients. Patients produced significantly more monomeric IgA1 antibodies than controls. These results show that patients with IgAN have a hyperresponsiveness limited to the subclass IgA1 and mainly expressed by an excess of monomers.

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