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Corrigendum Free access | 10.1172/JCI62188

Mice overexpressing BAFF develop a commensal flora–dependent, IgA-associated nephropathy

Douglas D. McCarthy, Julie Kujawa, Cheryl Wilson, Adrian Papandile, Urjana Poreci, Elisa A. Porfilio, Lesley Ward, Melissa A.E. Lawson, Andrew J. Macpherson, Kathy D. McCoy, York Pei, Lea Novak, Jeannette Y. Lee, Bruce A. Julian, Jan Novak, Ann Ranger, Jennifer L. Gommerman, and Jeffrey L. Browning

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Published February 1, 2012 - More info

Published in Volume 122, Issue 2 on February 1, 2012
J Clin Invest. 2012;122(2):778–778. https://doi.org/10.1172/JCI62188.
© 2012 The American Society for Clinical Investigation
Published February 1, 2012 - Version history
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Related article:

Mice overexpressing BAFF develop a commensal flora–dependent, IgA-associated nephropathy
Douglas D. McCarthy, … , Jennifer L. Gommerman, Jeffrey L. Browning
Douglas D. McCarthy, … , Jennifer L. Gommerman, Jeffrey L. Browning
Research Article Immunology

Mice overexpressing BAFF develop a commensal flora–dependent, IgA-associated nephropathy

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Abstract

B cell activation factor of the TNF family (BAFF) is a potent B cell survival factor. BAFF overexpressing transgenic mice (BAFF-Tg mice) exhibit features of autoimmune disease, including B cell hyperplasia and hypergammaglobulinemia, and develop fatal nephritis with age. However, basal serum IgA levels are also elevated, suggesting that the pathology in these mice may be more complex than initially appreciated. Consistent with this, we demonstrate here that BAFF-Tg mice have mesangial deposits of IgA along with high circulating levels of polymeric IgA that is aberrantly glycosylated. Renal disease in BAFF-Tg mice was associated with IgA, because serum IgA was highly elevated in nephritic mice and BAFF-Tg mice with genetic deletion of IgA exhibited less renal pathology. The presence of commensal flora was essential for the elevated serum IgA phenotype, and, unexpectedly, commensal bacteria–reactive IgA antibodies were found in the blood. These data illustrate how excess B cell survival signaling perturbs the normal balance with the microbiota, leading to a breach in the normal mucosal-peripheral compartmentalization. Such breaches may predispose the nonmucosal system to certain immune diseases. Indeed, we found that a subset of patients with IgA nephropathy had elevated serum levels of a proliferation inducing ligand (APRIL), a cytokine related to BAFF. These parallels between BAFF-Tg mice and human IgA nephropathy may provide a new framework to explore connections between mucosal environments and renal pathology.

Authors

Douglas D. McCarthy, Julie Kujawa, Cheryl Wilson, Adrian Papandile, Urjana Poreci, Elisa A. Porfilio, Lesley Ward, Melissa A.E. Lawson, Andrew J. Macpherson, Kathy D. McCoy, York Pei, Lea Novak, Jeannette Y. Lee, Bruce A. Julian, Jan Novak, Ann Ranger, Jennifer L. Gommerman, Jeffrey L. Browning

×

Original citation: J. Clin. Invest. 2011;121(10):3991–4002. doi:10.1172/JCI45563.

Citation for this corrigendum: J. Clin. Invest. 2012;122(2):778. doi:10.1172/JCI62188.

Figure 6A was inadvertently mislabeled. The correct figure appears below.

Figure 6

The authors regret the error.

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