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Journal ArticleDOI

Brain-immune connection: immuno-regulatory properties of CNS-resident cells.

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TLDR
This review considers properties of resident cells of the central nervous system, that participate in regulating the neural antigen (Ag)‐directed immune responses implicated in autoimmune diseases such as multiple sclerosis, in terms of events occurring within the CNS parenchyma and at the vascular interface.
Abstract
Even though the immune privileged status of the central nervous system (CNS) limits access of systemic immune cells through the blood brain barrier (BBB), an immune response can occur in this compartment with or without major breach of the BBB. In this review, we consider properties of resident cells of the CNS, that participate in regulating the neural antigen (Ag)-directed immune responses implicated in autoimmune diseases such as multiple sclerosis (MS). Under such conditions, the CNS is usually viewed as the target or victim of the immune assault, because such immune responses are thought to be initiated and regulated within the systemic immune compartment. The CNS-endogenous cells may themselves, however, initiate, regulate and sustain an immune response. We consider the immune regulatory functions within the CNS in terms of events occurring within the CNS parenchyma (microglia, astroglia) and at the vascular interface. These regulatory functions involve antigen presentation to T cells and polarization of the cytokine response of these cells. Such responses may contribute not only to the overall tissue injury in primary immune disorders but also in a wide range of traumatic, ischemic and degenerative processes.

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Citations
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Phagocytosis of Apoptotic Inflammatory Cells by Microglia and Its Therapeutic Implications: Termination of CNS Autoimmune Inflammation and Modulation by Interferon-Beta

TL;DR: The in vitro increase of phagocytosis by IFNβ merits further investigations whether this mechanism could also be therapeutically exploited.
Journal ArticleDOI

Metabolic and Inflammatory Adaptation of Reactive Astrocytes: Role of PPARs

TL;DR: The activation of selective PPAR isotype activity may serve as an input to better understand the role played by these receptors on the metabolic and inflammatory compensation of astrogliosis and might represent an opportunity to develop new therapeutic strategies against traumatic brain injuries and neurodegenerative diseases.
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Paraneoplastic Neurologic Disease Antigens: RNA-Binding Proteins and Signaling Proteins in Neuronal Degeneration

TL;DR: In this article, a model for the pathogenesis of paraneoplastic neurologic degeneration antigens is presented. And a model in which their functions are related to the pathogenic of autoimmune neurologic disease is discussed.
Journal ArticleDOI

Borna disease virus infection of the neonatal rat: developmental brain injury model of autism spectrum disorders.

TL;DR: The present review provides a detailed analysis of a new animal model of ASD that utilizes neonatal Borna disease virus infection of the rat brain as a unique experimental teratogen to study the pathogenesis of neurodevelopmental damage.
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Differential activation of microglia in neurogenic versus non‐neurogenic regions of the forebrain

TL;DR: The data show that both constitutive and postlesion levels of microglial activation differ between neurogenic and non‐neurogenic regions.
References
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Journal ArticleDOI

TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties.

TL;DR: Two types of cloned helper T cells are described, defined primarily by differences in the pattern of lymphokines ynthesized, and the different functions of the two types of cells and their lymphokine synthesis are discussed.
Journal Article

Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins.

TL;DR: A panel of antigen-specific mouse helper T cell clones was characterized according to patterns of lymphokine activity production, and two types of T cell were distinguished.
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Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl.

TL;DR: It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.
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Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma

TL;DR: Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.
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Annexin V for flow cytometric detection of phosphatidylserine expression on B cells undergoing apoptosis.

TL;DR: The results indicate that the phase in apoptosis that is characterized by chromatin condensation coincides with phosphatidylserine exposure, which precedes membrane damage that might lead to release from the cells of enzymes that are harmful to the surrounding tissues.
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