A new mouse model of anti-GBM disease sheds light on maternal transfer of alloantibodies in glomerular disease

Marina Vivarelli; Francesco Emma

doi:10.1016/j.kint.2019.08.007

A new mouse model of anti-GBM disease sheds light on maternal transfer of alloantibodies in glomerular disease

Kidney Int. 2019 Dec;96(6):1272-1274. doi: 10.1016/j.kint.2019.08.007.

Authors

Marina Vivarelli¹, Francesco Emma²

Affiliations

¹ Division of Nephrology, Department of Pediatric Subspecialties, Bambino Gesù Children's Hospital - IRCCS, Rome, Italy.
² Division of Nephrology, Department of Pediatric Subspecialties, Bambino Gesù Children's Hospital - IRCCS, Rome, Italy. Electronic address: [email protected].

PMID: 31759484
DOI: 10.1016/j.kint.2019.08.007

Abstract

Membranous nephropathy and anti-glomerular basement membrane glomerulonephritis are characterized by the deposition of antibodies that recognize specific glomerular epitopes. These antibodies may develop in autoimmune diseases, after exposure to new antigens or after passive maternal transfer, such as in neonatal membranous nephropathy secondary to in utero transfer of anti-neutral endopeptidase protein Igs. In this issue of Kidney International, Abrahamson et al. reported a murine model of passive anti-glomerular basement membrane disease caused by antibody transfer from pregnant mice to their offspring.

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MeSH terms

Animals
Anti-Glomerular Basement Membrane Disease*
Autoantibodies
Disease Models, Animal
Glomerulonephritis*
Humans
Immunoglobulin G
Isoantibodies
Laminin
Mice
Mice, Transgenic

Substances

Autoantibodies
Immunoglobulin G
Isoantibodies
Laminin
laminin alpha5