Author
Listed:
- Richard T. Strait
(Cincinnati Children’s Hospital Medical Center
University of Cincinnati College of Medicine)
- 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
Institute for Systemic Inflammation Research, University of Lübeck, 23538 Lübeck, Germany)
- 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
Cincinnati Children’s Hospital Medical Center)
- Fred D. Finkelman
(Cincinnati Children’s Hospital Medical Center
Allergy and Rheumatology, University of Cincinnati College of Medicine
Medical Service, Cincinnati Veterans Affairs Medical Center)
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.
Suggested Citation
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 , 2015.
"IgG1 protects against renal disease in a mouse model of cryoglobulinaemia,"
Nature, Nature, vol. 517(7535), pages 501-504, January.
Handle:
RePEc:nat:nature:v:517:y:2015:i:7535:d:10.1038_nature13868
DOI: 10.1038/nature13868
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