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
2017 ◽  
Vol 292 (42) ◽  
pp. 17449-17460 ◽  
Author(s):  
Jon A. Kenniston ◽  
Brandy M. Taylor ◽  
Gregory P. Conley ◽  
Janja Cosic ◽  
Kris J. Kopacz ◽  
...  

mAbs ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 848-860 ◽  
Author(s):  
Dilip K. Challa ◽  
Xiaoli Wang ◽  
Héctor Pérez Montoyo ◽  
Ramraj Velmurugan ◽  
Raimund J. Ober ◽  
...  

2019 ◽  
Vol 10 ◽  
Author(s):  
Felicity Kendrick ◽  
Neil D. Evans ◽  
Oscar Berlanga ◽  
Stephen J. Harding ◽  
Michael J. Chappell

2016 ◽  
Vol 84 (4) ◽  
pp. 237-244 ◽  
Author(s):  
E. G. de Souza ◽  
C. C. P. Hara ◽  
D. L. G. Fagundes ◽  
A. A. de Queiroz ◽  
G. Morceli ◽  
...  

Blood ◽  
2010 ◽  
Vol 116 (18) ◽  
pp. 3660-3668 ◽  
Author(s):  
Pingguo Chen ◽  
Conglei Li ◽  
Sean Lang ◽  
Guangheng Zhu ◽  
Adili Reheman ◽  
...  

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.


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

Lupus ◽  
2021 ◽  
pp. 096120332110450
Author(s):  
Ramdani Yanis ◽  
Cécile Bergua ◽  
Barbet Christelle ◽  
François Maillot ◽  
Adrien Bigot ◽  
...  

The neonatal Fc receptor (FcRn) is a ubiquitously expressed protein historically involved in IgG and albumin recycling. Recent data suggest an involvement in the pathophysiology of antibody-mediated autoimmune diseases. Among them, systemic lupus erythematosus (SLE) implies clinical and biological abnormalities of innate and adaptive circulating immune cells, potentially involving newly described functions of FcRn. In this study, FcRn expression was assessed by flow cytometry in peripheral blood leukocytes of 41 SLE patients with either active or inactive disease and 32 healthy donors. FcRn expression in B cells, natural killer cells, and T cells of SLE patients was statistically lower as compared to healthy donors. Conversely, FcRn level was statistically higher in non-classical monocyte subpopulations (CD14+CD16+ monocytes) of SLE patients versus healthy donors providing an interesting perspective to further explore its role in SLE pathophysiology.


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