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Myeloid Cell Heterogeneity in Health and Disease
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Myeloid Cell Heterogeneity in Health and Disease

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 (30 November 2019) | Viewed by 11482

Special Issue Editor

Dr. Andreas Weigert

E-Mail Website
Guest Editor
Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany
Interests: macrophage biology; cytokines; resolution of inflammation; tumor immunology; lipid signaling; apoptosis; innate-like lymphocytes; multispectral imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since their discovery by Élie Metchnikoff more than a century ago, it has become increasingly clear that myeloid cells are crucial guardians of homeostasis both under physiological and pathophysiological conditions. Myeloid cells belong to the innate immune system, comprising mononuclear (monocytes, macrophages, and dendritic cells (DCs)) and polymorphonuclear cells (neutrophils, eosinophils, basophils, and mast cells), as well as immature myeloid progenitors of both lineages summarized as myeloid-derived suppressor cells (MDSCs), which accumulate during inflammation. The vast functional diversity of myeloid cells, which is required to cope with their multitude of tasks during the steady-state and upon the disturbance of homeostasis, is not only due to their different lineage. They show remarkable intra-lineage phenotype plasticity resulting from differences in ontogeny, the specific requirements of their local microenvironment, and their extensive sensory repertoire that allows them to adapt rapidly to microenvironmental changes.

In this Special Issue of IJMS, authors are invited to submit their work on the molecular and biochemical mechanisms that govern the functional diversity of myeloid cells in health and disease, considering both pre-clinical and clinical settings. Both original papers and reviews on these widely-discussed topics are welcome.

Dr. Andreas Weigert
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.

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

  • Myeloid cells
  • Plasticity
  • Ontogeny
  • Microenvironment
  • Homeostasis
  • Inflammation
  • Phagocytes
  • Granulocytes

Published Papers (2 papers)

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Review

14 pages, 732 KiB  
Review
Interplay of Heme with Macrophages in Homeostasis and Inflammation
by Pooja Pradhan, Vijith Vijayan, Faikah Gueler and Stephan Immenschuh
Int. J. Mol. Sci. 2020, 21(3), 740; https://doi.org/10.3390/ijms21030740 - 23 Jan 2020
Cited by 30 | Viewed by 3970
Abstract
Macrophages are an integral part of the mononuclear phagocyte system that is critical for maintaining immune homeostasis. They play a key role for initiation and modulation of immunological responses in inflammation and infection. Moreover, macrophages exhibit a wide spectrum of tissue-specific phenotypes in [...] Read more.
Macrophages are an integral part of the mononuclear phagocyte system that is critical for maintaining immune homeostasis. They play a key role for initiation and modulation of immunological responses in inflammation and infection. Moreover, macrophages exhibit a wide spectrum of tissue-specific phenotypes in steady-state and pathophysiological conditions. Recent clinical and experimental evidence indicates that the ubiquitous compound heme is a crucial regulator of these cells, e.g., in the differentiation of monocytes to tissue-resident macrophages and/ or in activation by inflammatory stimuli. Notably, heme, an iron containing tetrapyrrole, is essential as a prosthetic group of hemoproteins (e.g., hemoglobin and cytochromes), whereas non-protein bound free or labile heme can be harmful via pro-oxidant, pro-inflammatory, and cytotoxic effects. In this review, it will be discussed how the complex interplay of heme with macrophages regulates homeostasis and inflammation via modulating macrophage inflammatory characteristics and/ or hematopoiesis. A particular focus will be the distinct roles of intra- and extracellular labile heme and the regulation of its availability by heme-binding proteins. Finally, it will be addressed how heme modulates macrophage functions via specific transcriptional factors, in particular the nuclear repressor BTB and CNC homologue (BACH)1 and Spi-C. Full article
(This article belongs to the Special Issue Myeloid Cell Heterogeneity in Health and Disease)
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16 pages, 1315 KiB  
Review
Age-Associated TET2 Mutations: Common Drivers of Myeloid Dysfunction, Cancer and Cardiovascular Disease
by Christina K. Ferrone, Mackenzie Blydt-Hansen and Michael J. Rauh
Int. J. Mol. Sci. 2020, 21(2), 626; https://doi.org/10.3390/ijms21020626 - 17 Jan 2020
Cited by 40 | Viewed by 7156
Abstract
Acquired, inactivating mutations in Tet methylcytosine dioxygenase 2 (TET2) are detected in peripheral blood cells of a remarkable 5%–10% of adults greater than 65 years of age. They impart a hematopoietic stem cell advantage and resultant clonal hematopoiesis of indeterminate potential [...] Read more.
Acquired, inactivating mutations in Tet methylcytosine dioxygenase 2 (TET2) are detected in peripheral blood cells of a remarkable 5%–10% of adults greater than 65 years of age. They impart a hematopoietic stem cell advantage and resultant clonal hematopoiesis of indeterminate potential (CHIP) with skewed myelomonocytic differentiation. CHIP is associated with an overall increased risk of transformation to a hematological malignancy, especially myeloproliferative and myelodysplastic neoplasms (MPN, MDS) and acute myeloid leukemia (AML), of approximately 0.5% to 1% per year. However, it is becoming increasingly possible to identify individuals at greatest risk, based on CHIP mutational characteristics. CHIP, and particularly TET2-mutant CHIP, is also a novel, significant risk factor for cardiovascular diseases, related in part to hyper-inflammatory, progeny macrophages carrying TET2 mutations. Therefore, somatic TET2 mutations contribute to myeloid expansion and innate immune dysregulation with age and contribute to prevalent diseases in the developed world—cancer and cardiovascular disease. Herein, we describe the impact of detecting TET2 mutations in the clinical setting. We also present the rationale and promise for targeting TET2-mutant and other CHIP clones, and their inflammatory environment, as potential means of lessening risk of myeloid cancer development and dampening CHIP-comorbid inflammatory diseases. Full article
(This article belongs to the Special Issue Myeloid Cell Heterogeneity in Health and Disease)
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