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Cytokines in Inflammatory Signaling 2.0
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Cytokines in Inflammatory Signaling 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1006

Special Issue Editors

Dr. Daniela Novick

E-Mail Website
Guest Editor
Department of Molecular Genetics, Weizmann Institute of Science Israel, Rehovot, Israel
Interests: inflammation; molecular biology; immunology; signaling pathways; biochemistry; autoimmune disease; cell biology; methods; Interleukin-18 (IL-18); IL-18 binding protein, cytokines and cytokines receptors
Special Issues, Collections and Topics in MDPI journals
Dr. Waipo Chong

E-Mail Website
Guest Editor
School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China
Interests: immunology; autoimmunity; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cytokines are produced by the host immune system for the control of microbial pathogens. They are involved in cell proliferation, survival, apoptosis, differentiation, and activation. However, their dysregulation can lead to undesired pathogenic inflammation and/or autoimmune diseases, such as multiple sclerosis, uveitis, rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus. This is achieved by activating various cell types, including fibroblasts, endothelial cells, epithelial cells, and immune cells, through different signalling pathways. Therefore, understanding the molecular mechanisms underlying the regulation of these cells by cytokines is important. This Special Issue aims to define the specific pathways that are influenced by cytokines during inflammation, as well as develop new therapeutics to more effectively target proinflammatory diseases.

Dr. Daniela Novick
Dr. Waipo Chong
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cytokines
  • inflammation
  • autoimmune diseases
  • immune homeostasis
  • signaling pathway
  • immunotherapy

Related Special Issue

Published Papers (2 papers)

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Research

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18 pages, 3289 KiB  
Article
Reduction in Hippocampal Amyloid-β Peptide (Aβ) Content during Glycine-Proline-Glutamate (Gly-Pro-Glu) Co-Administration Is Associated with Changes in Inflammation and Insulin-like Growth Factor (IGF)-I Signaling
by Laura M. Frago, Emma Burgos-Ramos, María Rodríguez-Pérez, Sandra Canelles, Eduardo Arilla-Ferreiro, Jesús Argente, Manuela G. López and Vicente Barrios
Int. J. Mol. Sci. 2024, 25(11), 5716; https://doi.org/10.3390/ijms25115716 - 24 May 2024
Viewed by 218
Abstract
Alzheimer’s disease (AD) is characterized by the deposition in the brain of senile plaques composed of amyloid-β peptides (Aβs) that increase inflammation. An endogenous peptide derived from the insulin-like growth factor (IGF)-I, glycine-proline-glutamate (GPE), has IGF-I-sensitizing and neuroprotective actions. Here, we examined the [...] Read more.
Alzheimer’s disease (AD) is characterized by the deposition in the brain of senile plaques composed of amyloid-β peptides (Aβs) that increase inflammation. An endogenous peptide derived from the insulin-like growth factor (IGF)-I, glycine-proline-glutamate (GPE), has IGF-I-sensitizing and neuroprotective actions. Here, we examined the effects of GPE on Aβ levels and hippocampal inflammation generated by the intracerebroventricular infusion of Aβ25-35 for 2 weeks (300 pmol/day) in ovariectomized rats and the signaling-related pathways and levels of Aβ-degrading enzymes associated with these GPE-related effects. GPE prevented the Aβ-induced increase in the phosphorylation of p38 mitogen-activated protein kinase and the reduction in activation of signal transducer and activator of transcription 3, insulin receptor substrate-1, and Akt, as well as on interleukin (IL)-2 and IL-13 levels in the hippocampus. The functionality of somatostatin, measured as the percentage of inhibition of adenylate cyclase activity and the levels of insulin-degrading enzyme, was also preserved by GPE co-treatment. These findings indicate that GPE co-administration may protect from Aβ insult by changing hippocampal cytokine content and somatostatin functionality through regulation of leptin- and IGF-I-signaling pathways that could influence the reduction in Aβ levels through modulation of levels and/or activity of Aβ proteases. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling 2.0)
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Review

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15 pages, 1509 KiB  
Review
Roles of Cytokines in Alzheimer’s Disease
by Zilin Chen, Yekkuni L. Balachandran, Wai Po Chong and Kannie W. Y. Chan
Int. J. Mol. Sci. 2024, 25(11), 5803; https://doi.org/10.3390/ijms25115803 - 26 May 2024
Viewed by 421
Abstract
The neuroimmune system is a collection of immune cells, cytokines, and the glymphatic system that plays a pivotal role in the pathogenesis and progression of Alzheimer’s disease (AD). Of particular focus are cytokines, a group of immune signaling molecules that facilitate communication among [...] Read more.
The neuroimmune system is a collection of immune cells, cytokines, and the glymphatic system that plays a pivotal role in the pathogenesis and progression of Alzheimer’s disease (AD). Of particular focus are cytokines, a group of immune signaling molecules that facilitate communication among immune cells and contribute to inflammation in AD. Extensive research has shown that the dysregulated secretion of certain cytokines (IL-1β, IL-17, IL-12, IL-23, IL-6, and TNF-α) promotes neuroinflammation and exacerbates neuronal damage in AD. However, anti-inflammatory cytokines (IL-2, IL-3, IL-33, and IL-35) are also secreted during AD onset and progression, thereby preventing neuroinflammation. This review summarizes the involvement of pro- and anti-inflammatory cytokines in AD pathology and discusses their therapeutic potential. Full article
(This article belongs to the Special Issue Cytokines in Inflammatory Signaling 2.0)
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