Muhammad Imran Arshad1, Hilal Ahmad Khan2, Gregory Noel3, Claire Piquet-Pellorce3, Michel Samson4. 1. Institut National de la Santé et de la Recherche Médicale (Inserm), Institut de Recherche Santé Environnement Travail (IRSET), Rennes, France; Université de Rennes 1, Rennes, France; Structure Fédérative BioSit UMS 3480 CNRS-US18 Inserm, Rennes, France; Institute of Microbiology, University of Agriculture, Faisalabad, Pakistan. 2. Institute of Microbiology, University of Agriculture, Faisalabad, Pakistan. 3. Institut National de la Santé et de la Recherche Médicale (Inserm), Institut de Recherche Santé Environnement Travail (IRSET), Rennes, France; Université de Rennes 1, Rennes, France; Structure Fédérative BioSit UMS 3480 CNRS-US18 Inserm, Rennes, France. 4. Institut National de la Santé et de la Recherche Médicale (Inserm), Institut de Recherche Santé Environnement Travail (IRSET), Rennes, France; Université de Rennes 1, Rennes, France; Structure Fédérative BioSit UMS 3480 CNRS-US18 Inserm, Rennes, France. Electronic address: michel.samson@univ-rennes1.fr.
Abstract
PURPOSE: The purpose of this review was to examine the comprehensively accumulated data regarding potential therapeutic aspects of exogenous administration of interleukin 33 (IL-33) or its antagonists in allergic, cancerous, infectious, and inflammatory diseases. METHODS: A selected review was undertaken of publications that examined the protective and exacerbating effects of IL-33 or its inhibitors in different diseases. Mechanisms of action are summarized to examine the putative role of IL-33 in various diseases. FINDINGS: IL-33 promoted antibacterial, antiviral, anti-inflammatory, and vaccine adjuvant functions. However, in TH2-biased respiratory, allergic, parasitic, and inflammatory conditions, IL-33 exhibited disease-sensitizing effects. The alarmin cytokine IL-33 induced protective effects in diseases via recruitment of regulatory T cells; antiviral CD8(+) cells, natural killer cells, γδ T cells, and nuocytes; antibacterial and antifungal neutrophils or macrophages; vaccine-associated B/T cells; and inhibition of nuclear factor-κB-mediated gene transcription. In contrast, IL-33 exacerbated the disease process by increasing TH2 cytokines, IgE and eosinophilic immune responses, and inhibition of leukocyte recruitment in various diseases. IMPLICATIONS: The protective or exacerbated aspects of use of IL-33 or its inhibitors are dependent on the type of infection or inflammatory condition, duration of disease (acute or chronic), organ involved, cytokine microenvironment, dose or kinetics of IL-33, and genetic predisposition. The alarmin cytokine IL-33 acts at cellular, molecular, and transcriptional levels to mediate pluripotent functions in various diseases and has potential therapeutic value to mitigate the disease process.
PURPOSE: The purpose of this review was to examine the comprehensively accumulated data regarding potential therapeutic aspects of exogenous administration of interleukin 33 (IL-33) or its antagonists in allergic, cancerous, infectious, and inflammatory diseases. METHODS: A selected review was undertaken of publications that examined the protective and exacerbating effects of IL-33 or its inhibitors in different diseases. Mechanisms of action are summarized to examine the putative role of IL-33 in various diseases. FINDINGS:IL-33 promoted antibacterial, antiviral, anti-inflammatory, and vaccine adjuvant functions. However, in TH2-biased respiratory, allergic, parasitic, and inflammatory conditions, IL-33 exhibited disease-sensitizing effects. The alarmin cytokine IL-33 induced protective effects in diseases via recruitment of regulatory T cells; antiviral CD8(+) cells, natural killer cells, γδ T cells, and nuocytes; antibacterial and antifungal neutrophils or macrophages; vaccine-associated B/T cells; and inhibition of nuclear factor-κB-mediated gene transcription. In contrast, IL-33 exacerbated the disease process by increasing TH2 cytokines, IgE and eosinophilic immune responses, and inhibition of leukocyte recruitment in various diseases. IMPLICATIONS: The protective or exacerbated aspects of use of IL-33 or its inhibitors are dependent on the type of infection or inflammatory condition, duration of disease (acute or chronic), organ involved, cytokine microenvironment, dose or kinetics of IL-33, and genetic predisposition. The alarmin cytokine IL-33 acts at cellular, molecular, and transcriptional levels to mediate pluripotent functions in various diseases and has potential therapeutic value to mitigate the disease process.
Authors: Christoph Bergmann; Aurélie Poli; Ioana Agache; Rodolfo Bianchini; Heather J Bax; Mariana Castells; Silvia Crescioli; David Dombrowicz; Denisa Ferastraoaru; Edda Fiebiger; Hannah J Gould; Karin Hartmann; Elena Izquierdo; Galateja Jordakieva; Debra H Josephs; Marek Jutel; Francesca Levi-Schaffer; Leticia de Las Vecillas; Michael T Lotze; Gabriel Osborn; Mariona Pascal; Frank Redegeld; David Rosenstreich; Franziska Roth-Walter; Carsten Schmidt-Weber; Mohamed Shamji; Esther H Steveling; Michelle C Turner; Eva Untersmayr; Erika Jensen-Jarolim; Sophia N Karagiannis Journal: Allergy Date: 2022-03-14 Impact factor: 14.710
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