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Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 985646, 13 pages
http://dx.doi.org/10.1155/2012/985646
Review Article

IgG Placental Transfer in Healthy and Pathological Pregnancies

1Departamento de Pediatria, Faculdade de Medicina, Universidade de São Paulo, Av. Dr. Enéas Carvalho de Aguiar, 647, Cerqueira César, São Paulo, SP 05403-900, Brazil
2Laboratório de Investigação Médica (LIM-36), Instituto da Criança, Hospital das Clínicas, Av. Dr. Enéas Carvalho de Aguiar, 647, Cerqueira César, São Paulo, SP 05403-900, Brazil
3Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof. Lineu Prestes, 1374, Cidade Universitária, São Paulo, SP 05508-000, Brazil

Received 30 June 2011; Accepted 24 July 2011

Academic Editor: Andres Salumets

Copyright © 2012 Patricia Palmeira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Placental transfer of maternal IgG antibodies to the fetus is an important mechanism that provides protection to the infant while his/her humoral response is inefficient. IgG is the only antibody class that significantly crosses the human placenta. This crossing is mediated by FcRn expressed on syncytiotrophoblast cells. There is evidence that IgG transfer depends on the following: (i) maternal levels of total IgG and specific antibodies, (ii) gestational age, (iii) placental integrity, (iv) IgG subclass, and (v) nature of antigen, being more intense for thymus-dependent ones. These features represent the basis for maternal immunization strategies aimed at protecting newborns against neonatal and infantile infectious diseases. In some situations, such as mothers with primary immunodeficiencies, exogenous IgG acquired by intravenous immunoglobulin therapy crosses the placenta in similar patterns to endogenous immunoglobulins and may also protect the offspring from infections in early life. Inversely, harmful autoantibodies may cross the placenta and cause transitory autoimmune disease in the neonate.