IgG1 protects against renal disease in a mouse model of cryoglobulinaemia

Richard T. Strait, Monica T. Posgai, Ashley Mahler, Nathaniel Barasa, Chaim O. Jacob, Jörg Köhl, Marc Ehlers, Keith Stringer, Shiva Kumar Shanmukhappa, David Witte, Md Monir Hossain, Marat Khodoun, Andrew B. Herr and Fred D. Finkelman ()
Additional contact information
Richard T. Strait: Cincinnati Children’s Hospital Medical Center
Monica T. Posgai: Biochemistry and Microbiology, University of Cincinnati College of Medicine
Ashley Mahler: Cincinnati Children’s Hospital Medical Center
Nathaniel Barasa: Cincinnati Children’s Hospital Medical Center
Chaim O. Jacob: University of Southern California School of Medicine
Jörg Köhl: Cincinnati Children’s Hospital Medical Center
Marc Ehlers: Institute for Systemic Inflammation Research, University of Lübeck, 23538 Lübeck, Germany
Keith Stringer: Cincinnati Children’s Hospital Medical Center
Shiva Kumar Shanmukhappa: Cincinnati Children’s Hospital Medical Center
David Witte: Cincinnati Children’s Hospital Medical Center
Md Monir Hossain: Cincinnati Children’s Hospital Medical Center
Marat Khodoun: Allergy and Rheumatology, University of Cincinnati College of Medicine
Andrew B. Herr: Biochemistry and Microbiology, University of Cincinnati College of Medicine
Fred D. Finkelman: Cincinnati Children’s Hospital Medical Center

Nature, 2015, vol. 517, issue 7535, 501-504

Abstract: Here, the predominant murine immunoglobulin G subclass, IgG1, which is a poor activator of effector mechanisms, is shown to have a regulatory function, protecting against the development of IgG3 immune-complex-driven renal disease by competing with IgG3 for antigen and increasing immune complex solubility.

Date: 2015
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DOI: 10.1038/nature13868

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