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Journal ArticleDOI

Cytokine networks in neuroinflammation

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TLDR
Recent observations on the impact of dysregulated cytokine networks in neuroinflammation are summarized.
Abstract
Cytokines provide cells with the ability to communicate with one another and orchestrate complex multicellular behaviour. There is an emerging understanding of the role that cytokines play in normal homeostatic tissue function and how dysregulation of these cytokine networks is associated with pathological conditions. The central nervous system (CNS), where few blood-borne immune cells circulate, seems to be particularly vulnerable to dysregulated cytokine networks. In degenerative diseases, such as proteopathies, CNS-resident cells are the predominant producers of pro-inflammatory cytokines. By contrast, in classical neuroinflammatory diseases, such as multiple sclerosis and encephalitides, pro-inflammatory cytokines are mainly produced by tissue-invading leukocytes. Whereas the effect of dysregulated cytokine networks in proteopathies is controversial, cytokines delivered to the CNS by invading immune cells are in general detrimental to the tissue. Here, we summarize recent observations on the impact of dysregulated cytokine networks in neuroinflammation.

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Citations
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Establishing the therapeutic potential of the P2X7 receptor ion channel in amyotrophic lateral sclerosis

Anjila Dongol
TL;DR: The author and the views expressed in this thesis are those of the author and do not necessarily represent the views of the University of Wollongong.
Book ChapterDOI

An In Vitro Blood-Brain Barrier Model to Study Firm Shear Stress-Resistant Leukocyte Adhesion to Human Brain Endothelial Cells.

TL;DR: An in vitro technique to study the interaction between human leukocytes with human brain endothelial cells under shear stress mimicking the blood flow in vivo, coupled to live-cell imaging is described.
Posted ContentDOI

High permeability of the CSF flow in the juvenile mouse brain by brain-wide DCE-MRI

TL;DR: In this paper, the authors visualized the whole-head signal of gadolinium contrast agents in mouse brains to investigate the CSF flow from the signals of Gd-contrast agents using magnetic resonance imaging (MRI) in the course of developmental stages.
Journal ArticleDOI

Convergent mechanisms of microglia-mediated synaptic dysfunction contribute to diverse neuropathological conditions.

TL;DR: In this article , early microglial changes, driven by genetic alterations coupled with environmental neuro-immune modulation, may be a common denominator that contributes to early synaptic pathologies, highlighting their importance as broadly relevant therapeutic targets within neurological diseases.
Journal ArticleDOI

The Physio-Pathological Role of Group I Metabotropic Glutamate Receptors Expressed by Microglia in Health and Disease with a Focus on Amyotrophic Lateral Sclerosis

TL;DR: The role of group I metabotropic glutamate receptors (mGluRs) in shaping microglia cells' phenotype in specific physio-pathological conditions, including some neurodegenerative disorders, was discussed in this article .
References
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Journal ArticleDOI

Systematic Review: Process of Forming Academic Service Partnerships to Reform Clinical Education

TL;DR: This study’s findings can provide practical guidelines to steer partnership programs within the academic and clinical bodies, with the aim of providing a collaborative partnership approach to clinical education.
Journal ArticleDOI

The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

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Journal ArticleDOI

Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

TL;DR: Findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
Journal ArticleDOI

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

TL;DR: In vivo, antibody to IL- 17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused Chemokine production and leukocyte infiltration, indicating a unique T helper lineage that regulates tissue inflammation.
Journal ArticleDOI

IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

TL;DR: Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.
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