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Metabolic Reprogramming of Immune Cells in Tumor Microenvironment

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 8185

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Special Issue Editor

Dr. Deepika Awasthi

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Guest Editor

Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, NY 10065, USA
Interests: oxidative stress; neutrophil extracellular traps; cell metabolism, immune cells; dietary fats; ER stress; cancers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent advances over the last decade in understanding cellular metabolism has brought the field of immunometabolism to the forefront. The complex nature of tumor microenvironment is characterized by low pH, hypoxic conditions, as well as the depletion of crucial nutrients (such as glucose, glutamine, amino acids and fatty acids. This results in a tug-of-war for the available nutrients between immune and cancer cells and a state of “metabolic competition”. These metabolic adaptations in tumor and immune cells may induce new physiological links and potential immunoregulatory pathways. Moreover, current research in this field has helped to tune metabolic pathways, in both cancer cells and immune cells, representing an indispensable determinant of the cell’s decision towards its viability, differentiation, function, and even fate. In this Special Issue, we invite researchers to contribute their valuable work on this exciting and intriguing field “immunometabolism”. We seek interesting research on the role of metabolic pathways and cellular metabolites (such as tryptophan, lactate, and cholesterols), in relation to immune cells that are integral part of anti- or pro-tumor responses (such as T cells, B cells, macrophages, DCs, and MDSCs).

Dr. Deepika Awasthi
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. Current Issues in Molecular Biology 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 2200 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

cellular metabolism
metabolic reprogramming
immunometabolism
tumor microenvironment
immunotherapy
metabolites
immunosuppression
immune cells
tumor cells

Published Papers (4 papers)

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Research

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21 pages, 2610 KiB

Open AccessArticle

Expressions of Type I and III Interferons, Endogenous Retroviruses, TRIM28, and SETDB1 in Children with Respiratory Syncytial Virus Bronchiolitis

by Pier-Angelo Tovo, Silvia Garazzino, Francesco Savino, Valentina Daprà, Giulia Pruccoli, Maddalena Dini, Giacomo Filisetti, Elisa Funiciello, Ilaria Galliano and Massimiliano Bergallo

Curr. Issues Mol. Biol. 2023, 45(2), 1197-1217; https://doi.org/10.3390/cimb45020079 - 2 Feb 2023

Cited by 1 | Viewed by 2196

Abstract

Interferons (IFNs) and IFN-stimulated genes (ISGs) play essential roles for the control of viral infections. Their expression in infants with respiratory syncytial virus (RSV) bronchiolitis is poorly defined. Human endogenous retroviruses (HERVs) represent 8% of our genome and modulate inflammatory and immune reactions. TRIM28 and SETDB1 participate in the epigenetic regulation of genes involved in the immune response, including IFNs and HERVs. No study has explored the expression of HERVs, TRIM28, and SETDB1 during RSV bronchiolitis. We assessed, through a PCR real-time Taqman amplification assay, the transcription levels of six IFN-I ISGs, four IFNλs, the pol genes of HERV-H, -K, and -W families, the env genes of Syncytin (SYN)1 and SYN2, and of TRIM28/SETDB1 in whole blood from 37 children hospitalized for severe RSV bronchiolitis and in healthy children (HC). The expression of most IFN-I ISGs was significantly higher in RSV+ patients than in age-matched HC, but it was inhibited by steroid therapy. The mRNA concentrations of IFN-λs were comparable between patients and age-matched HC. This lack of RSV-driven IFN-III activation may result in the defective protection of the airway mucosal surface leading to severe bronchiolitis. The expression of IFN-III showed a positive correlation with age in HC, that could account for the high susceptibility of young children to viral respiratory tract infections. The transcription levels of every HERV gene were significantly lower in RSV+ patients than in HC, while the expressions of TRIM28/SETDB1 were overlapping. Given the negative impact of HERVs and the positive effects of TRIM28/SETDB1 on innate and adaptive immune responses, the downregulation of the former and the normal expression of the latter may contribute to preserving immune functions against infection. Full article

(This article belongs to the Special Issue Metabolic Reprogramming of Immune Cells in Tumor Microenvironment)

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11 pages, 839 KiB

Open AccessArticle

Protective Effect of Vitamin D against Hepatic Molecular Apoptosis Caused by a High-Fat Diet in Rats

by Huda F. Alshaibi, Sherin Bakhashab, Asma Almuhammadi, Yusuf S. Althobaiti, Mohammed A. Baghdadi and Khadeejah Alsolami

Curr. Issues Mol. Biol. 2023, 45(1), 479-489; https://doi.org/10.3390/cimb45010031 - 5 Jan 2023

Cited by 2 | Viewed by 1960

Abstract

The protective effects of vitamin D (VitD) in different diseases were studied. The liver is of great interest, especially with the presence of VitD receptors. A high-fat diet (HFD) is associated with many diseases, including liver injury. Consumption of saturated fatty acids triggers hepatic apoptosis and is associated with increased inflammation. We aimed in this study to investigate the protective effects of VitD on hepatic molecular apoptotic changes in response to an HFD in rats. Forty male Wistar albino rats were used and divided into four groups: control, HFD, control + VitD, and VitD-supplemented HFD (HFD + VitD) groups. After six months, the rats were sacrificed, and the livers were removed. RNA was extracted from liver tissues and used for the quantitative real-time RT-PCR of different genes: B-cell lymphoma/leukemia-2 (BCL2), BCL-2-associated X protein (Bax), Fas cell surface death receptor (FAS), FAS ligand (FASL), and tumor necrosis factor α (TNF-α). The results showed that an HFD increased the expression of the pro-apoptotic genes Bax, FAS, and FASL, and reduced the expression of the anti-apoptotic gene BCL2. Interestingly, a VitD-supplemented HFD significantly increased the BCL2 expression and decreased the expression of all pro-apoptotic genes and TNFα. In conclusion, VitD has a protective role against hepatic molecular apoptotic changes in response to an HFD. Full article

(This article belongs to the Special Issue Metabolic Reprogramming of Immune Cells in Tumor Microenvironment)

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11 pages, 661 KiB

Open AccessArticle

Glutathione and Its Metabolic Enzymes in Gliomal Tumor Tissue and the Peritumoral Zone at Different Degrees of Anaplasia

by Larisa Obukhova, Tatiana Kopytova, Elena Murach, Natalya Shchelchkova, Claudia Kontorshchikova, Igor Medyanik, Natalia Orlinskaya, Artem Grishin, Michael Kontorshchikov and Dariya Badanina

Curr. Issues Mol. Biol. 2022, 44(12), 6439-6449; https://doi.org/10.3390/cimb44120439 - 19 Dec 2022

Cited by 1 | Viewed by 1743

Abstract

This research was aimed at investigating the features of free radical activity and the parameters of glutathione metabolism in tumor tissues and the peritumoral zone at different degrees of glial tumor anaplasia. We analyzed postoperative material from 20 patients with gliomas of different degrees of anaplasia. The greatest differences compared to adjacent noncancerous tissues were found in the tumor tissue: an increased amount of glutathione and glutathione-related enzymes at Grades I and II, and a decrease of these parameters at Grades III and IV. For the peritumoral zone of Grades I and II, the indices changed in different directions, while for Grades III and IV, they occurred synchronously with the tumor tissue changes. For Low Grade and High Grade gliomas, opposite trends were revealed regarding changes in the level of glutathione and the enzymes involved in its metabolism and in the free radical activity in the peritumoral zone. The content of glutathione and the enzymes involved in its metabolism decreased with the increasing degree of glioma anaplasia. In contrast, free radical activity increased. The glutathione system is an active participant in the antioxidant defense of the body and can be used to characterize the cell condition of gliomas at different stages of tumor development. Full article

(This article belongs to the Special Issue Metabolic Reprogramming of Immune Cells in Tumor Microenvironment)

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Review

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15 pages, 1930 KiB

Open AccessReview

Metabolic Interplay in the Tumor Microenvironment: Implications for Immune Function and Anticancer Response

by Reem Youssef, Rohan Maniar, Jaffar Khan and Hector Mesa

Curr. Issues Mol. Biol. 2023, 45(12), 9753-9767; https://doi.org/10.3390/cimb45120609 - 5 Dec 2023

Cited by 1 | Viewed by 1582

Abstract

Malignant tumors exhibit rapid growth and high metabolic rates, similar to embryonic stem cells, and depend on aerobic glycolysis, known as the “Warburg effect”. This understanding has enabled the use of radiolabeled glucose analogs in tumor staging and therapeutic response assessment via PET scans. Traditional treatments like chemotherapy and radiotherapy target rapidly dividing cells, causing significant toxicity. Despite immunotherapy’s impact on solid tumor treatment, gaps remain, leading to research on cancer cell evasion of immune response and immune tolerance induction via interactions with the tumor microenvironment (TME). The TME, consisting of immune cells, fibroblasts, vessels, and the extracellular matrix, regulates tumor progression and therapy responses. TME-targeted therapies aim to transform this environment from supporting tumor growth to impeding it and fostering an effective immune response. This review examines the metabolic disparities between immune cells and cancer cells, their impact on immune function and therapeutic targeting, the TME components, and the complex interplay between cancer cells and nontumoral cells. The success of TME-targeted therapies highlights their potential to achieve better cancer control or even a cure. Full article

(This article belongs to the Special Issue Metabolic Reprogramming of Immune Cells in Tumor Microenvironment)

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