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The Interleukin-1 Superfamily: Molecular Mechanisms of Action in Health and Pathology

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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: closed (15 September 2022) | Viewed by 14928

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Special Issue Editor

Dr. Vladimir V. Sharoyko

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1. Department of Biomedicinal Chemistry, Institute of Chemistry, Saint Petersburg State University, 199034 Saint Petersburg, Russia
2. Department of General and Bioorganic Chemistry, First Pavlov Saint Petersburg State Medical University, 199034 Saint Petersburg, Russia
Interests: biochemistry; bioorganic chemistry; medicine chemistry; cell and molecular biology; biomimetic materials; pharmacytes; click chemistry; hybrid materials; carbon nanomaterials; nanotechnology; theranostics; drug delivery; anticancer agents; tumor microenvironment; inflammation; molecular metabolism; signal transduction; mitochondria; oxidative stress; DNA damage; bioassays; biomolecular interactions; isothermal titration calorimetry; fluorescence thermal shift; flow cytofluorimetry; biological activity of compounds; cancer; diabetes; preclinical animal models
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Special Issue Information

Dear Colleagues,

The IL-1 superfamily is a group of 11 cytokines that induce a complex network of pro-inflammatory cytokines and, through the expression of integrins on leukocytes and endothelial cells, regulate and initiate inflammatory responses. The IL-1 family of ligands and receptors is primarily associated with acute and chronic inflammation. The IL-1 family includes 7 ligands with agonist activity (IL-1α and β, IL-18, IL-33, IL-36α, β, γ), three receptor antagonists (IL-1Ra, IL-36Ra, IL-38), and an anti-inflammatory cytokine (IL-37). IL-1 is extensively produced by tissue macrophages, monocytes, fibroblasts, and dendritic cells, but is also expressed by B lymphocytes, NK cells, microglia, and epithelial cells. The IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases. A better understanding of the pathophysiology of the IL-1 superfamily has the potential to lead to innovative therapeutic tools and targets.

This Special Issue of the International Journal of Molecular Sciences is open to both original research articles and review articles focusing on molecular mechanisms of action IL-1 family members and advances in preclinical evaluation of pharmacologic approaches.

Dr. Vladimir V. Sharoyko
Guest Editor

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.

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Keywords

IL-1 superfamily
ligands with agonist activity
receptor antagonists
anti-inflammatory cytokine
pathophysiology of the IL-1 superfamily
innovative therapeutic tools and targets

Published Papers (4 papers)

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Research

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34 pages, 5594 KiB

Open AccessArticle

Interactions between the NLRP3-Dependent IL-1β and the Type I Interferon Pathways in Human Plasmacytoid Dendritic Cells

by Dóra Bencze, Tünde Fekete, Walter Pfliegler, Árpád Szöőr, Eszter Csoma, Antónia Szántó, Tünde Tarr, Attila Bácsi, Lajos Kemény, Zoltán Veréb and Kitti Pázmándi

Int. J. Mol. Sci. 2022, 23(20), 12154; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012154 - 12 Oct 2022

Cited by 1 | Viewed by 2077

Abstract

Generally, a reciprocal antagonistic interaction exists between the antiviral type I interferon (IFN) and the antibacterial nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing 3 (NLRP3)-dependent IL-1β pathways that can significantly shape immune responses. Plasmacytoid dendritic cells (pDCs), as professional type I IFN-producing cells, are the major coordinators of antiviral immunity; however, their NLRP3-dependent IL-1β secretory pathway is poorly studied. Our aim was to determine the functional activity of the IL-1β pathway and its possible interaction with the type I IFN pathway in pDCs. We found that potent nuclear factor-kappa B (NF-κB) inducers promote higher levels of pro-IL-1β during priming compared to those activation signals, which mainly trigger interferon regulatory factor (IRF)-mediated type I IFN production. The generation of cleaved IL-1β requires certain secondary signals in pDCs and IFN-α or type I IFN-inducing viruses inhibit IL-1β production of pDCs, presumably by promoting the expression of various NLRP3 pathway inhibitors. In line with that, we detected significantly lower IL-1β production in pDCs of psoriasis patients with elevated IFN-α levels. Collectively, our results show that the NLRP3-dependent IL-1β secretory pathway is inducible in pDCs; however, it may only prevail under inflammatory conditions, in which the type I IFN pathway is not dominant. Full article

(This article belongs to the Special Issue The Interleukin-1 Superfamily: Molecular Mechanisms of Action in Health and Pathology)

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25 pages, 5930 KiB

Open AccessArticle

Divalent Metal Transporter 1 Knock-Down Modulates IL-1β Mediated Pancreatic Beta-Cell Pro-Apoptotic Signaling Pathways through the Autophagic Machinery

by Taewook Kang, Honggang Huang, Thomas Mandrup-Poulsen and Martin R. Larsen

Int. J. Mol. Sci. 2021, 22(15), 8013; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158013 - 27 Jul 2021

Cited by 4 | Viewed by 2556

Abstract

Pro-inflammatory cytokines promote cellular iron-import through enhanced divalent metal transporter-1 (DMT1) expression in pancreatic β-cells, consequently cell death. Inhibition of β-cell iron-import by DMT1 silencing protects against apoptosis in animal models of diabetes. However, how alterations of signaling networks contribute to the protective action of DMT1 knock-down is unknown. Here, we performed phosphoproteomics using our sequential enrichment strategy of mRNA, protein, and phosphopeptides, which enabled us to explore the concurrent molecular events in the same set of wildtype and DMT1-silenced β-cells during IL-1β exposure. Our findings reveal new phosphosites in the IL-1β-induced proteins that are clearly reverted by DMT1 silencing towards their steady-state levels. We validated the levels of five novel phosphosites of the potential protective proteins using parallel reaction monitoring. We also confirmed the inactivation of autophagic flux that may be relevant for cell survival induced by DMT1 silencing during IL-1β exposure. Additionally, the potential protective proteins induced by DMT1 silencing were related to insulin secretion that may lead to improving β-cell functions upon exposure to IL-1β. This global profiling has shed light on the signal transduction pathways driving the protection against inflammation-induced cell death in β-cells after DMT1 silencing. Full article

(This article belongs to the Special Issue The Interleukin-1 Superfamily: Molecular Mechanisms of Action in Health and Pathology)

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Review

Jump to: Research

29 pages, 1678 KiB

Open AccessReview

The Role of the Interleukin-1 Family in Complications of Prematurity

by Elys A. Green, Steven P. Garrick, Briana Peterson, Philip J. Berger, Robert Galinsky, Rod W. Hunt, Steven X. Cho, Jane E. Bourke, Marcel F. Nold and Claudia A. Nold-Petry

Int. J. Mol. Sci. 2023, 24(3), 2795; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032795 - 01 Feb 2023

Cited by 9 | Viewed by 4000

Abstract

Preterm birth is a major contributor to neonatal morbidity and mortality. Complications of prematurity such as bronchopulmonary dysplasia (BPD, affecting the lung), pulmonary hypertension associated with BPD (BPD-PH, heart), white matter injury (WMI, brain), retinopathy of prematurity (ROP, eyes), necrotizing enterocolitis (NEC, gut) and sepsis are among the major causes of long-term morbidity in infants born prematurely. Though the origins are multifactorial, inflammation and in particular the imbalance of pro- and anti-inflammatory mediators is now recognized as a key driver of the pathophysiology underlying these illnesses. Here, we review the involvement of the interleukin (IL)-1 family in perinatal inflammation and its clinical implications, with a focus on the potential of these cytokines as therapeutic targets for the development of safe and effective treatments for early life inflammatory diseases. Full article

(This article belongs to the Special Issue The Interleukin-1 Superfamily: Molecular Mechanisms of Action in Health and Pathology)

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35 pages, 7363 KiB

Open AccessReview

The Therapeutic Prospects of Targeting IL-1R1 for the Modulation of Neuroinflammation in Central Nervous System Disorders

by João P. Luís, Carlos J. V. Simões and Rui M. M. Brito

Int. J. Mol. Sci. 2022, 23(3), 1731; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031731 - 02 Feb 2022

Cited by 12 | Viewed by 5422

Abstract

The interleukin-1 receptor type 1 (IL-1R1) holds pivotal roles in the immune system, as it is positioned at the “epicenter” of the inflammatory signaling networks. Increased levels of the cytokine IL-1 are a recognized feature of the immune response in the central nervous system (CNS) during injury and disease, i.e., neuroinflammation. Despite IL-1/IL-1R1 signaling within the CNS having been the subject of several studies, the roles of IL-1R1 in the CNS cellular milieu still cause controversy. Without much doubt, however, the persistent activation of the IL-1/IL-1R1 signaling pathway is intimately linked with the pathogenesis of a plethora of CNS disease states, ranging from Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS), all the way to schizophrenia and prion diseases. Importantly, a growing body of evidence is showing that blocking IL-1R1 signaling via pharmacological or genetic means in different experimental models of said CNS diseases leads to reduced neuroinflammation and delayed disease progression. The aim of this paper is to review the recent progress in the study of the biological roles of IL-1R1, as well as to highlight key aspects that render IL-1R1 a promising target for the development of novel disease-modifying treatments for multiple CNS indications. Full article

(This article belongs to the Special Issue The Interleukin-1 Superfamily: Molecular Mechanisms of Action in Health and Pathology)

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