IgG Placental Transfer in Healthy and Pathological Pregnancies

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.

Genome-wide association study identifies common variants at TNFRSF13B associated with IgG level in a healthy Chinese male population

“…1 As the only isotype that can pass through the human placenta, IgG is able to protect the fetus in utero. 2 Meanwhile, IgG gets involved in chronic inflammatory processes contributed to the destruction of healthy tissues in autoimmune diseases, such as arthritis and systemic lupus erythematosus. 3 Serum IgG level varies considerably from one person to another, 4 but little when testing the same person repeatedly.…”

Review of immunological and virological aspects as contributory factors in Sudden Unexpected Death in Infancy (SUDI)

“…Before birth, the sterile uterine environment offers little antigen exposure [37]. In the neonatal period infants are dependent on their innate immune mechanisms for protection against pathogens and rely on maternally transferred antibodies for limited adaptive immune protection.…”

“…This offers some protection against infectious disease, but impaired responses in a substantial number of infants lead to susceptibility to disease. Antibody responses in infants are typically shorter, delayed and respond with lower immunoglobulin (Ig) G2 expression with lower affinity to specific antigens than those found in adults [37,38].…”

“…Fewer neutrophils are present in babies and their neutrophils and monocytes also respond sub-optimally to chemo-attractants [37]. Between birth and 1 month, monocytes from infants generate less interferon (IFN)-α, IFN-γ and interleukin (IL)-12p70 than adults, although 9 production increases rapidly from birth to 2 years of age.…”

“…Early infancy is further marked by low numbers of effector memory B cells (CD27 + ) and effector memory T cells (CD45RA -CD45RO + ). Although cytokines in infants seem to be less polyfunctional than in adults, they are key components in the regulation of innate and adaptive immune responses to viral infections through interference with viral entry and replication [37,38,39].…”