Iron scavenging and myeloid cell polarization.

hemolysis macrophages multiple sclerosis neuroinflammation sickle cell disease tumor microenvironment

Journal

Trends in immunology
ISSN: 1471-4981
Titre abrégé: Trends Immunol
Pays: England
ID NLM: 100966032

Informations de publication

Date de publication:
24 Jul 2024
Historique:
received: 05 06 2024
revised: 25 06 2024
accepted: 27 06 2024
medline: 26 7 2024
pubmed: 26 7 2024
entrez: 25 7 2024
Statut: aheadofprint

Résumé

Myeloid cells that populate all human organs and blood are a versatile class of innate immune cells. They are crucial for sensing and regulating processes as diverse as tissue homeostasis and inflammation and are frequently characterized by their roles in either regulating or promoting inflammation. Recent studies in cultured cells and mouse models highlight the role of iron in skewing the functional properties of myeloid cells in tissue damage and repair. Here, we review certain emerging concepts on how iron influences and determines myeloid cell polarization in the context of its uptake, storage, and metabolism, including in conditions such as multiple sclerosis (MS), sickle cell disease, and tumors.

Identifiants

pubmed: 39054114
pii: S1471-4906(24)00155-8
doi: 10.1016/j.it.2024.06.006
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Natalie Ludwig (N)

Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Interdisciplinary Center for Neurosciences, Heidelberg University, Heidelberg, Germany.

Stefania Cucinelli (S)

Department of Paediatric Hematology, Oncology, and Immunology, University of Heidelberg, Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), European Molecular Biology Laboratory and University of Heidelberg, Heidelberg, Germany.

Simon Hametner (S)

Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria; Medical Neuroscience Cluster, Medical University of Vienna, Vienna, Austria.

Martina U Muckenthaler (MU)

Department of Paediatric Hematology, Oncology, and Immunology, University of Heidelberg, Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), European Molecular Biology Laboratory and University of Heidelberg, Heidelberg, Germany; German Centre for Cardiovascular Research (DZHK), Partner site Heidelberg/Mannheim, Heidelberg, Germany; Translational Lung Research Center Heidelberg (TLRC), German Center for Lung Research (DZL), University of Heidelberg, Heidelberg, Germany. Electronic address: martina.muckenthaler@med.uni-heidelberg.de.

Lucas Schirmer (L)

Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Interdisciplinary Center for Neurosciences, Heidelberg University, Heidelberg, Germany; Mannheim Center for Translational Neuroscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Electronic address: lucas.schirmer@medma.uni-heidelberg.de.

Classifications MeSH