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Published on: July 8, 2020
Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy
Douglas D McCarthy1, Julie Kujawa, Cheryl Wilson
1Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
The Journal of Clinical Investigation
|September 2, 2011
Summary
Excessive B cell survival signaling from BAFF overexpression disrupts the gut microbiota balance, leading to elevated IgA and kidney disease in mice. This suggests a link between mucosal immunity and non-mucosal autoimmune conditions like IgA nephropathy.
Area of Science:
- Immunology
- Nephrology
- Microbiome research
Background:
- B cell activation factor (BAFF) is crucial for B cell survival and implicated in autoimmune diseases.
- BAFF-transgenic (BAFF-Tg) mice develop autoimmune features, including nephritis, but elevated IgA suggests complex pathology.
Purpose of the Study:
- To investigate the role of IgA in BAFF-induced renal pathology.
- To explore the connection between BAFF, microbiota, and IgA dysregulation.
- To identify potential parallels with human IgA nephropathy.
Main Methods:
- Analysis of BAFF-Tg mice with and without IgA.
- Assessment of serum IgA levels and glycosylation.
- Investigation of the role of commensal flora in IgA elevation.
- Comparison of BAFF-Tg mice findings with human IgA nephropathy patient data.
Main Results:
- BAFF-Tg mice exhibit mesangial IgA deposits and elevated polymeric IgA.
- Renal pathology is reduced in BAFF-Tg mice lacking IgA.
- Commensal bacteria-reactive IgA is found in the blood, dependent on gut flora.
- Elevated APRIL, a BAFF-related cytokine, is observed in some IgA nephropathy patients.
Conclusions:
- Overabundant BAFF signaling disrupts mucosal-peripheral compartmentalization via IgA.
- This dysregulation may link microbiota imbalance to non-mucosal immune diseases like nephritis.
- Findings suggest BAFF-Tg mice offer a model for studying IgA nephropathy and mucosal-renal connections.
