scholarly journals Structural basis for pH-insensitive inhibition of immunoglobulin G recycling by an anti-neonatal Fc receptor antibody

2017 ◽  
Vol 292 (42) ◽  
pp. 17449-17460 ◽  
Author(s):  
Jon A. Kenniston ◽  
Brandy M. Taylor ◽  
Gregory P. Conley ◽  
Janja Cosic ◽  
Kris J. Kopacz ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Fc Receptor ◽  
Structural Basis ◽  
Neonatal Fc Receptor ◽  
Receptor Antibody

scholarly journals Parameter Identification for a Model of Neonatal Fc Receptor-Mediated Recycling of Endogenous Immunoglobulin G in Humans

2019 ◽  
Vol 10 ◽  
Author(s):  
Felicity Kendrick ◽  
Neil D. Evans ◽  
Oscar Berlanga ◽  
Stephen J. Harding ◽  
Michael J. Chappell
Keyword(s):  
Parameter Identification ◽  
Immunoglobulin G ◽  
Fc Receptor ◽  
Neonatal Fc Receptor

Animal model of fetal and neonatal immune thrombocytopenia: role of neonatal Fc receptor in the pathogenesis and therapy

Blood ◽  
2010 ◽  
Vol 116 (18) ◽  
pp. 3660-3668 ◽  
Author(s):  
Pingguo Chen ◽  
Conglei Li ◽  
Sean Lang ◽  
Guangheng Zhu ◽  
Adili Reheman ◽  
...  
Keyword(s):  
Animal Model ◽  
Immunoglobulin G ◽  
Immune Thrombocytopenia ◽  
Fc Receptor ◽  
Maternal Antibodies ◽  
Severe Bleeding ◽  
Neonatal Fc Receptor ◽  
Igg Isotypes ◽  
Β3 Integrin

Abstract Fetal and neonatal immune thrombocytopenia (FNIT) is a severe bleeding disorder in which maternal antibodies cross the placenta and destroy fetal/neonatal platelets. It has been demonstrated that the neonatal Fc receptor (FcRn) regulates immunoglobulin G (IgG) homeostasis and plays an important role in transplacental IgG transport. However, the role of FcRn in the pathogenesis and therapy of FNIT has not been studied. Here, we developed an animal model of FNIT using combined β3 integrin–deficient and FcRn-deficient (β3−/−FcRn−/−) mice. We found that β3−/−FcRn−/− mice are immunoresponsive to β3+/+FcRn−/− platelets. The generated antibodies were β3 integrin specific and were maintained at levels that efficiently induced thrombocytopenia in adult β3+/+FcRn−/− mice. FNIT was observed when immunized β3−/−FcRn+/+ females were bred with β3+/+FcRn+/+ males, while no FNIT occurred in β3−/−FcRn−/− females bred with β3+/+FcRn−/− males, suggesting that FcRn is indispensable for the induction of FNIT. We further demonstrated that fetal FcRn was responsible for the transplacental transport of various IgG isotypes. We found that anti-FcRn antibody and intravenous IgG prevented FNIT, and that intravenous IgG ameliorated FNIT through both FcRn-dependent and -independent pathways. Our data suggest that targeting FcRn may be a potential therapy for human FNIT as well as other maternal pathogenic antibody-mediated diseases.

scholarly journals Structural basis of pH-dependent antibody binding by the neonatal Fc receptor

Structure ◽  
1998 ◽  
Vol 6 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Daniel E Vaughn ◽  
Pamela J Bjorkman
Keyword(s):  
Fc Receptor ◽  
Antibody Binding ◽  
Structural Basis ◽  
Neonatal Fc Receptor ◽  
Ph Dependent

scholarly journals How the controller is controlled ? neonatal Fc receptor expression and immunoglobulin G homeostasis

Immunology ◽  
2007 ◽  
Vol 120 (2) ◽  
pp. 145-147 ◽  
Author(s):  
Shuo-Wang Qiao ◽  
Wayne I. Lencer ◽  
Richard S. Blumberg
Keyword(s):  
Immunoglobulin G ◽  
Fc Receptor ◽  
Receptor Expression ◽  
Neonatal Fc Receptor

Neonatal Fc Receptor and its Role in the Absorption, Distribution, Metabolism and Excretion of Immunoglobulin G-Based Biotherapeutics

2013 ◽  
Vol 14 (7) ◽  
pp. 764-790 ◽  
Author(s):  
Craig Giragossian ◽  
Tracey Clark ◽  
Nicole Piché-Nicholas ◽  
Christopher Bowman
Keyword(s):  
Immunoglobulin G ◽  
Fc Receptor ◽  
Neonatal Fc Receptor
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