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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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Regulatory T Cells Restrain Pathogenic T Helper Cells during Skin Inflammation.

TL;DR: A non-redundant role of Treg cells restraining skin inflammation and mediating skin homeostasis is identified, identified using the Aldara-skin inflammation model in combination with the inducible depletion of Foxp3+ T Reg cells.
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Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.

TL;DR: In this article, a review focusing on the recent advancement in understanding molecular mechanisms of neuroinflammation and its role in the etiopathogenesis of various neurological disorders, especially Alzheimer's disease (AD), Parkinson disease (PD), and Epilepsy, is presented.
Journal ArticleDOI

The 10,000 Immunomes Project: Building a Resource for Human Immunology.

TL;DR: The 10KIP is presented, a framework for growing a diverse human immunology reference, from ImmPort, a publicly available resource of subject-level immunology data, and variations in serum cytokines and leukocytes by age, race, and sex are described.
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Brain dysfunction in COVID-19 and CAR-T therapy: cytokine storm-associated encephalopathy.

TL;DR: In this article, the authors investigated whether COVID-19-related encephalopathy, ICANS, and other encephalopathies associated with cytokine storm, share clinical and investigative findings.
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.
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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

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