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Review
.2020 Oct 6:36:441-468.
doi: 10.1146/annurev-cellbio-021120-033518. Epub 2020 Jul 28.

The Role of Immune Factors in Shaping Fetal Neurodevelopment

Affiliations
Review

The Role of Immune Factors in Shaping Fetal Neurodevelopment

Alice Lu-Culligan et al. Annu Rev Cell Dev Biol..

Abstract

Fetal neurodevelopment in utero is profoundly shaped by both systemic maternal immunity and local processes at the maternal-fetal interface. Immune pathways are a critical participant in the normal physiology of pregnancy and perturbations of maternal immunity due to infections during this period have been increasingly linked to a diverse array of poor neurological outcomes, including diseases that manifest much later in postnatal life. While experimental models of maternal immune activation (MIA) have provided groundbreaking characterizations of the maternal pathways underlying pathogenesis, less commonly examined are the immune factors that serve pathogen-independent developmental functions in the embryo and fetus. In this review, we explore what is known about the in vivo role of immune factors in fetal neurodevelopment during normal pregnancy and provide an overview of how MIA perturbs the proper orchestration of this sequence of events. Finally, we discuss how the dysregulation of immune factors may contribute to the manifestation of a variety of neurological disorders.

Keywords: complement; cytokines; immune system; maternal immune activation; neurodevelopment; pregnancy.

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Figures

Figure 1
Figure 1
Fetal neurodevelopment and MIA throughout the timeline of murine pregnancy. Gestational age is denoted by embryonic day (E) starting at E0.5, designated as the morning that the seminal plug is observed. Postnatal day (P) 0 is designated as the day of birth. Immune pathways are known to participate in normal physiological processes of brain formation and development. The timing, character, and intensity of MIA relative to the timing of development dictate fetal vulnerability to a spectrum of neurological diseases. Abbreviations: AD, Alzheimer’s disease; ASD, autism spectrum disorder; CP, cerebral palsy; MIA, maternal immune activation; NTD, neural tube defect; PD, Parkinson’s disease; TLR, Toll-like receptor. Figure adapted from images created withBiorender.com.
Figure 2
Figure 2
MIA alters immune programs at the maternal–fetal interface to directly impact fetal neurodevelopment. Various maternal conditions (e.g., inflammation, infection, autoimmune disease) can lead to perturbations in immune factor expression at the maternal–fetal interface, leading to disruptions in neurodevelopment. Abbreviations: CNS, central nervous system; MIA, maternal immune activation; TLR, Toll-like receptor. Figure adapted from images created withBiorender.com.
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