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.read more
Citations
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Journal ArticleDOI
Next Generation Precision Medicine: CRISPR-mediated Genome Editing for the Treatment of Neurodegenerative Disorders
Sudhanshu P. Raikwar,Nidhi Shankar Kikkeri,Ragha Chaitanya Sakuru,Daniyal Saeed,Haris Zahoor,Keerthivaas Premkumar,Shireen Mentor,Shireen Mentor,Ramasamy Thangavel,Ramasamy Thangavel,Iuliia Dubova,Iuliia Dubova,Mohammad Ejaz Ahmed,Mohammad Ejaz Ahmed,Govindhasamy Pushpavathi Selvakumar,Govindhasamy Pushpavathi Selvakumar,Duraisamy Kempuraj,Duraisamy Kempuraj,Smita Zaheer,Shankar S. Iyer,Shankar S. Iyer,Asgar Zaheer,Asgar Zaheer +22 more
TL;DR: The scientific community is urged to maintain high scientific and ethical standards and utilize CRISPR for developing in vitro disease in a dish model, in vivo testing in nonhuman primates and lower vertebrates and for the development of neurotherapeutics for the currently incurable neurodegenerative disorders.
Journal ArticleDOI
A Pivotal Role for Thiamine Deficiency in the Expression of Neuroinflammation Markers in Models of Alcohol-Related Brain Damage.
TL;DR: Data suggest an overt brain inflammatory response by TD and a subtle change by CET alone, which leads to unique regional and temporal profiles of induction of neuroimmune genes.
Journal ArticleDOI
Utility of chemokines CCL2, CXCL8, 10 and 13 and interleukin 6 in the pediatric cohort for the recognition of neuroinflammation and in the context of traditional cerebrospinal fluid neuroinflammatory biomarkers.
TL;DR: The increased CSF level of CXCL13 was the marker with the greatest predictive utility for the general recognition of neuroinflammation among all of the individually investigated biomarkers and the potential clinical utility of chemo/cytokines in the differential diagnosis of neuroinflammatory diseases was identified.
Journal ArticleDOI
Evaluation of the effect of GM-CSF blocking on the phenotype and function of human monocytes
TL;DR: It is shown that anti-GM-CSF treatment induces modulatory monocytes that act in a CXCL-11-dependent manner, a mechanism that can be used in the development of novel approaches to treat chronic inflammatory autoimmune diseases.
Book ChapterDOI
Neuroinflammation in organophosphate-induced neurotoxicity
Michelle Guignet,Pamela J. Lein +1 more
TL;DR: This chapter summarizes the evidence documenting that not only acute OP intoxication but also repeated subclinical OP exposures elicit neuroinflammatory responses and reviews the available evidence suggesting that neuroinflammation may contribute to the pathogenesis of OP neurotoxicity and/or neuroprotective mechanisms triggered in response to OP-induced injury.
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
John Hardy,Dennis J. Selkoe +1 more
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
Laurie E. Harrington,Robin D. Hatton,Paul R. Mangan,Henrietta Turner,Theresa L. Murphy,Kenneth M. Murphy,Casey T. Weaver +6 more
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
Heon Park,Zhaoxia Li,Xuexian O. Yang,Seon Hee Chang,Roza Nurieva,Yi Hong Wang,Ying Wang,Leroy Hood,Zhou Zhu,Qiang Tian,Chen Dong +10 more
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
Claire L. Langrish,Yi Yi Chen,Wendy M. Blumenschein,Jeanine D. Mattson,Beth Basham,Jonathan D. Sedgwick,Terrill K. McClanahan,Robert A. Kastelein,Daniel J. Cua +8 more
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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