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Maternal IgG Affects Brain Development of Mouse Pups

ABSTRACT: Maternal IgG is an immunoglobulin present in breast milk and has been shown to play a role in the development of the immune system in infants. The aim of this study was to investigate the effects of maternal IgG on brain development in mouse pups. Maternal IgG immunoreactivity was observed in microglial cells of the pup brain, peaking at postnatal 8 day. In particular, strong IgG immunoreactivity was observed in the microglia in the corpus callosum and cerebellar white matter. IgG stimulation of primary cultured microglia resulted in activation of the type I interferon feedback loop by Syk. Among the IgG subclasses, IgG2a was found to have a strong influence on microglia. Analysis of FcRn KO mice that were unable to take up IgG from their mothers revealed that these mice had abnormalities in the proliferation and/or survival of microglia, oligodendrocytes, and some types of interneurons. FcRn KO mice also exhibited abnormalities in social behavior and adaptation to novel environments. This study suggests that maternal IgG affects brain development in pups.

ORGANISM(S): Mus musculus

PROVIDER: GSE248310 | GEO | 2024/05/24

REPOSITORIES: GEO

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Project description:The transplacental transfer of maternal IgG to the developing fetus is critical for infant protection against infectious pathogens in the first year of life. However, factors that modulate the transplacental transfer efficiency of maternal IgG that could be harnessed for maternal vaccine design remain largely undefined. HIV-infected women have impaired placental IgG transfer, yet the mechanism underlying this impaired transfer is unknown, presenting an opportunity to explore factors that contribute to the efficiency of placental IgG transfer. We measured the transplacental transfer efficiency of maternal HIV and other pathogen-specific IgG in historical U.S. (n=120) and Malawian (n=47) cohorts of HIV-infected mothers and their HIV58 exposed uninfected and HIV-infected infants. We then examined the role of maternal HIV disease progression, infant factors, placental Fc receptor expression, and IgG Fc region subclass and glycan signatures and their association with transplacental transfer efficiency of maternal antigen-specific IgG. We established 3 distinct phenotypes of placental IgG transfer efficiency in HIV-infected women, including: 1) efficient transfer of the majority of antigen-specific IgG populations; 2) generally poor IgG transfer phenotype that was strongly associated with maternal CD4+ T cell counts, hypergammaglobulinemia, and frequently yielded non-protective levels of vaccine-specific IgG; and 3) variable transfer of IgG across distinct antigen specificities. Interestingly, maternal IgG characteristics, such as binding to placentally expressed Fc receptors FcgRIIa and FcgRIIIa, IgG subclass frequency, and Fc region glycan profiles were associated with placental IgG transfer efficiency. These maternal IgG transplacental transfer determinants were distinct among different antigen-specific IgG populations. Our findings suggest that in HIV-infected women, both maternal disease progression and Fc region characteristics modulate the selective placental transfer of distinct IgG subpopulations, with implications for both the health of HIV-exposed uninfected infants and maternal vaccine design.

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Maternal IgG Affects Brain Development of Mouse Pups

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