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Novel roles for immune molecules in neural development: implications for neurodevelopmental disorders

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TLDR
These functions for immune molecules during neural development suggest that they could also mediate pathological responses to chronic elevations of cytokines in neurodevelopmental disorders, including autism spectrum disorders (ASD) and schizophrenia.
Abstract
Although the brain has classically been considered “immune-privileged”, current research suggests an extensive communication between the immune and nervous systems in both health and disease. Recent studies demonstrate that immune molecules are present at the right place and time to modulate the development and function of the healthy and diseased central nervous system (CNS). Indeed, immune molecules play integral roles in the CNS throughout neural development, including affecting neurogenesis, neuronal migration, axon guidance, synapse formation, activity-dependent refinement of circuits, and synaptic plasticity. Moreover, the roles of individual immune molecules in the nervous system may change over development. This review focuses on the effects of immune molecules on neuronal connections in the mammalian central nervous system – specifically the roles for MHCI and its receptors, complement, and cytokines on the function, refinement, and plasticity of geniculate, cortical and hippocampal synapses, and their relationship to neurodevelopmental disorders. These functions for immune molecules during neural development suggest that they could also mediate pathological responses to chronic elevations of cytokines in neurodevelopmental disorders, including autism spectrum disorders (ASD) and schizophrenia.

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Sex differences in microglial colonization of the developing rat brain

TL;DR: In this paper, the authors demonstrate that the number and morphology of microglia throughout development is dependent upon the sex and age of the individual, as well as the brain region of interest, and that gene expression of a large number of cytokines, chemokines and their receptors shifts dramatically over development, and is highly dependent upon sex.
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The immune system and developmental programming of brain and behavior

TL;DR: The goal of this review is to describe the important role of the immune system during brain development, and to discuss some of the many ways in which immune activation during early brain development can affect the later-life outcomes of neural function, immune function, mood and cognition.
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Immune mediators in the brain and peripheral tissues in autism spectrum disorder

TL;DR: Findings indicate that the immune system is a point of convergence for multiple ASD-related genetic and environmental risk factors.
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Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development.

TL;DR: Testing protein levels of cytokines in the blood and three brain regions from offspring of poly(I:C)- and saline-injected mice at five postnatal ages indicates that MIA leads to long-lasting, region-specific changes in brain cytokine changes in offspring that may alter CNS development and behavior.
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Sex differences in neurodevelopmental and neurodegenerative disorders: Focus on microglial function and neuroinflammation during development

TL;DR: Understanding the mechanisms behind sex differences in disease progression could help develop more targeted therapy with higher success rate, especially in diseases where sex differences are most prominent.
References
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Book

Cellular and Molecular Immunology

TL;DR: Cellular and molecular immunology , Cellular and molecular Immunology , کتابخانه الکرونیک و دیجیتال - آذرسا
Book

Immunobiology: The Immune System in Health and Disease

TL;DR: Introductory immunology textbook for medical students, advanced undergraduates, and graduate students.
Journal ArticleDOI

Synaptic Activity and the Construction of Cortical Circuits

TL;DR: The sequential combination of spontaneously generated and experience-dependent neural activity endows the brain with an ongoing ability to accommodate to dynamically changing inputs during development and throughout life.
Journal ArticleDOI

The classical complement cascade mediates CNS synapse elimination.

TL;DR: It is shown that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina, supporting a model in which unwanted synapses are tagged by complement for elimination and suggesting that complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.
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