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Metabolism of Immune Cells: Applications in Health and Disease

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A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (20 September 2021) | Viewed by 6670

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Special Issue Editors

Dr. Sarah Dimeloe

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Guest Editor

Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, IBR, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
Interests: metabolism of immune cells; Immunology; metabolism; interlinked immune function; T lymphocytes

Dr. Nicholas Jones

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Guest Editor

Institute of Life Science, Swansea University Medical School, Swansea University, Swansea SA2 8PP, UK
Interests: metabolism

Special Issue Information

Dear Colleagues,

Over the last decade, research into the metabolism of immune cells, or “immunometabolism”, has revealed many novel ways in which metabolic processes intimately support the function of innate and adaptive immune cells. Our understanding now extends beyond the role of metabolism in generating biosynthetic intermediates and energy in these cells, to an appreciation of how it controls epigenetic, transcriptional, and translational pathways to determine cell phenotype and protective (or pathological) function. Indeed, alongside these fundamental discoveries, translational research has revealed that immune cell metabolism is frequently dysregulated in chronic diseases including cancer, infection, and autoimmunity.

Taken together, these mechanistic and clinical studies highlight the exciting potential for targeting dysfunctional immune cell metabolism to treat such diseases, and it is now time to evaluate the potential for translating this knowledge into novel therapies. This Special Issue of Metabolites will focus on the role of immune cell metabolism in health and disease and the potential therapeutic applications of this area of research. We welcome high-quality original research articles providing insight into the dysregulation of immune cell metabolism in disease, or supporting novel therapeutic approaches to target this. We also invite the submission of review articles providing novel perspectives on this exciting area of research.

Dr. Sarah Dimeloe
Dr. Nicholas Jones
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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

immunometabolism
metabolomics

Published Papers (2 papers)

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Research

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10 pages, 4768 KiB

Open AccessArticle

Disruption of GPR35 Signaling in Bone Marrow-Derived Cells Does Not Influence Vascular Inflammation and Atherosclerosis in Hyperlipidemic Mice

by Roland Baumgartner, Felipe B. Casagrande, Randi B. Mikkelsen, Martin Berg, Konstantinos A. Polyzos, Maria J. Forteza, Aastha Arora, Thue W. Schwartz, Siv A. Hjorth and Daniel F. J. Ketelhuth

Metabolites 2021, 11(7), 411; https://doi.org/10.3390/metabo11070411 - 23 Jun 2021

Cited by 7 | Viewed by 2405

Abstract

G-protein-coupled receptor-35 (GPR35) has been identified as a receptor for the tryptophan metabolite kynurenic acid (KynA) and suggested to modulate macrophage polarization in metabolic tissues. Whether GPR35 can influence vascular inflammation and atherosclerosis has however never been tested. Lethally irradiated LdlrKO mice were randomized to receive GPR35KO or wild type (WT) bone marrow transplants and fed a high cholesterol diet for eight weeks to develop atherosclerosis. GPR35KO and WT chimeric mice presented no difference in the size of atherosclerotic lesions in the aortic arch (2.37 ± 0.58% vs. 1.95 ± 0.46%, respectively) or in the aortic roots (14.77 ± 3.33% vs. 11.57 ± 2.49%, respectively). In line with these data, no changes in the percentage of VCAM-1+, IA^b + cells, and CD3+ T cells, as well as alpha smooth muscle cell actin expression, was observed between groups. Interestingly, the GPR35KO group presented a small but significant increase in CD68+ macrophage infiltration in the plaque. However, in vitro culture experiments using bone marrow-derived macrophages from both groups indicated that GPR35 plays no role in modulating the secretion of major inflammatory cytokines. Our study indicates that GPR35 expression does not play a direct role in macrophage activation, vascular inflammation, and the development of atherosclerosis. Full article

(This article belongs to the Special Issue Metabolism of Immune Cells: Applications in Health and Disease)

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Review

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19 pages, 779 KiB

Open AccessReview

Immunometabolic Therapeutic Targets of Graft-versus-Host Disease (GvHD)

by Kudakwashe Mhandire, Komalpreet Saggu and Nataliya Prokopenko Buxbaum

Metabolites 2021, 11(11), 736; https://doi.org/10.3390/metabo11110736 - 27 Oct 2021

Cited by 7 | Viewed by 3850

Abstract

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a curative option in the treatment of aggressive malignant and non-malignant blood disorders. However, the benefits of allo-HSCT can be compromised by graft-versus-host disease (GvHD), a prevalent and morbid complication of allo-HSCT. GvHD occurs when donor immune cells mount an alloreactive response against host antigens due to histocompatibility differences between the donor and host, which may result in extensive tissue injury. The reprogramming of cellular metabolism is a feature of GvHD that is associated with the differentiation of donor CD4+ cells into the pathogenic Th1 and Th17 subsets along with the dysfunction of the immune-suppressive protective T regulatory cells (Tregs). The activation of glycolysis and glutaminolysis with concomitant changes in fatty acid oxidation metabolism fuel the anabolic activities of the proliferative alloreactive microenvironment characteristic of GvHD. Thus, metabolic therapies such as glycolytic enzyme inhibitors and fatty acid metabolism modulators are a promising therapeutic strategy for GvHD. We comprehensively review the role of cellular metabolism in GvHD pathogenesis, identify candidate therapeutic targets, and describe potential strategies for augmenting immunometabolism to ameliorate GvHD. Full article

(This article belongs to the Special Issue Metabolism of Immune Cells: Applications in Health and Disease)

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