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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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Minocycline Ameliorates Chronic Unpredictable Mild Stress-Induced Neuroinflammation and Abnormal mPFC-HIPP Oscillations in Mice

TL;DR: It is revealed that microglia is critically involved in stress-induced neuroinflammation, which may underlie the molecular mechanism of CUMS-induced anxiety behavior.
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Role of Inflammatory Cytokines in the Conversion of Mild Cognitive Im- pairment to Dementia: A Prospective Study.

TL;DR: ACT levels have a significant predictive value in the conversion of MCI to dementia and could be a protective factor, and serum concentrations of several subclinical inflammatory markers were determined.
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High interleukin-8 and/or extracellular signal-regulated kinase 2 expression predicts poor prognosis in patients with hepatocellular carcinoma.

TL;DR: A significant increase in the risk of recurrence and mortality in HCC patients with high expression levels of IL-8 and/or ERK2 is indicated, compared with patients with low expression, which may be predictors of postoperative prognosis in patients with HCC.
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LXW7 attenuates inflammation via suppressing Akt/nuclear factor kappa B and mitogen-activated protein kinases signaling pathways in lipopolysaccharide-stimulated BV2 microglial cells.

TL;DR: The present study's findings suggest that LXW7 has a substantial therapeutic potential for treating inflammatory and neurodegenerative diseases and may be associated with the inhibition of microglial activation via Akt/NF-κB and JNK/MAPK signaling pathways by blocking integrin αvβ3 receptor.
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Current understanding of plant-derived exosome-like nanoparticles in regulating the inflammatory response and immune system microenvironment.

TL;DR: In this article , a review summarizes the biogenesis, composition, and classification of exosomes, the common separation, purification, and characterization methods of PELNs, the potential advantages of plant-derived exosome-like nanoparticles over ADEs, and the anti-inflammatory and immunomodulatory functions of Pels in various diseases including colitis, cancer, and inflammation-associated metabolic diseases.
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.
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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
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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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