scispace - formally typeset
Journal ArticleDOI

Cytokine networks in neuroinflammation

Reads0
Chats0
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.

read more

Citations
More filters
Journal ArticleDOI

Heparan Sulfate Proteoglycans as Relays of Neuroinflammation

TL;DR: This review focuses on recent discoveries regarding the role of HSPGs, HS, and heparanase during inflammation, with particular focus on the brain, and how current knowledge could be applied to augment HS-mediated events during sustained neuroinflammation, which contributes to neurodegeneration in AD.
Journal ArticleDOI

Microglia, Cytokines, and Neural Activity: Unexpected Interactions in Brain Development and Function.

TL;DR: In this article, the same signaling pathways that regulate inflammatory responses to injury and disease outside of the brain also play powerful roles in brain development, plasticity, and function, raising the question of how the same signalling molecules can play such distinct roles in peripheral tissues compared to the central nervous system, a system previously thought to be largely protected from inflammatory signaling.
Journal ArticleDOI

Graphene Quantum Dots' Surface Chemistry Modulates the Sensitivity of Glioblastoma Cells to Chemotherapeutics.

TL;DR: It is shown that surface chemistry modulates GQDs’ biocompatibility and can be adopted as a suitable delivery and therapeutic strategy for the treatment of glioblastoma by both directly destabilizing the cell membrane and indirectly increasing the efficacy of chemotherapeutic drugs.
Journal ArticleDOI

Quantum dot cellular uptake and toxicity in the developing brain: implications for use as imaging probes

TL;DR: It is found that QD behavior is highly dependent on surface functionality and that treatment of cultured organotypic whole hemisphere slices with QDs results in dose-dependent toxicity and metallothionein increase, but no subsequent mRNA expression level changes in inflammatory cytokines or other oxidative stress.
Book ChapterDOI

Ethanol and Cytokines in the Central Nervous System.

TL;DR: This chapter focuses on key cytokines and chemokines that mediate the ethanol-induced neuroimmune responses and uses IL-1β, as an example cytokine, to discuss the neuromodulatory properties of cytokines on cellular properties and synaptic transmission.
References
More filters
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

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.
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.
Related Papers (5)

Neuroinflammation in Alzheimer's disease

Michael T. Heneka, +41 more
- 01 Apr 2015 -