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.
Highlights
Anti-infectious fetal protection is provided by several factors acting together
This has been reported in several works performed in certain regions of Africa showing lower cord/maternal placental transfer ratios of total immunoglobulin G (IgG), indicating that this limitation of active placental transfer of antibodies is related to the higher maternal IgG levels common in Africa [41,42,43]
It has been demonstrated that in term neonates with a low birth weight, all IgG subclasses were transferred with reduced efficiency, but IgG1 and IgG2 subclasses were transferred with significantly less efficiency than IgG3 and IgG4
Summary
Anti-infectious fetal protection is provided by several factors acting together. The uterine cavity contains innate immune detection and effector systems that maintain sterility, detect infection and, under conditions of substantial microbial invasion, induce expression of mediators that could accelerate lung maturation and induce a preterm labor to deliver the fetus from a threatening environment [1]. Infant blood monocytes produce less IFN-α, IFN-γ, and IL-12 subunit p70 (IL-12 p70) than cells obtained from adults Production of these cytokines rapidly increases between birth and 1 or 2 years of age. Neonatal T CD4+ cells present an intrinsic immaturity with a diminished capacity to generate memory cells and reduced Th1 effector functions such as the production of less IFN-γ and lower CD40L expression. These deficiencies seem mainly to be related to the fact that the cells are still naive, having met few antigens [7]. Additional immune response support is given by the mother through breast milk, which contains functional nutrients and IgA antibodies that provide efficient protection directly after birth by preventing adherence of infectious agents on the mucosal membranes and their entrance into tissues
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