Signaling Networks and Gene Expression in Immune Cells

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 3724

Special Issue Editors


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Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: gene expression; transcriptional regulation; macrophage activation; immunometabolism

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Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: macrophage activation; cell signaling; immunometabolism; gene expression; transcriptional regulation; mitochondria; epigenetic mechanisms
Special Issues, Collections and Topics in MDPI journals

E-Mail
Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: transcriptional regulation; post-transcriptional regulation; miRNA; splicing mechanisms; liver
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immune cells fight against infections and sustain cell integrity and homeostasis by initiating and orchestrating finely tuned immune responses to manifold internal and external triggers, including pathogens and cytokines. Innate and adaptive immune responses are shaped by intricate signaling networks. In relation to this, the fascinating and rapidly evolving field of immunometabolism depicts the impact of metabolites, enzymes, and pathways on immune system plasticity in both quiescence and activation. During immune cell activation, metabolism becomes highly adaptable to promptly provide necessary materials according to the organism's requirements. Metabolic processes provide nutrients and energy and also contribute to gene expression reprogramming and transcription of multiple signal proteins. The metabolic and transcriptional profiles drive the development of various immune cell subsets. Indeed, metabolic signaling is closely related to epigenetic and, in turn, gene expression changes in both innate and adaptive immune cells. There is a large body of evidence on how aberrant immunometabolism contributes to immune dysfunction and diseases like cancer and chronic inflammatory disorders such as diabetes, obesity, atherosclerosis, and rheumatoid arthritis.

For our upcoming Special Issue, we invite researchers to contribute their valuable work, whether original research or review articles, on the most recent findings of signaling networks, including immunometabolic pathways and mechanisms of gene expression in immune cells. We further encourage contributions that delve into the regulation, mechanisms, pathways, gene expression reprogramming, cell types, and mediators involved in the interplay between immunity and metabolism, as well as emerging therapies.

Dr. Santarsiero Anna
Dr. Vittoria Infantino
Dr. Paolo Convertini
Guest Editors

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Keywords

  • cell signaling
  • immunometabolism
  • metabolic reprogramming
  • immunity
  • innate immune cells
  • adaptive immunity
  • transcriptional/post-transcriptional regulation
  • gene expression
  • inflammatory process
  • inflammatory diseases

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Published Papers (3 papers)

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Research

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15 pages, 2499 KiB  
Article
Transcriptional Regulation and Function of Malic Enzyme 1 in Human Macrophage Activation
by Anna Santarsiero, Simona Todisco, Paolo Convertini, Chiara De Leonibus and Vittoria Infantino
Biomedicines 2024, 12(9), 2089; https://doi.org/10.3390/biomedicines12092089 - 13 Sep 2024
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Abstract
Macrophages represent primary players of the innate immune system. Macrophage activation triggers several signaling pathways and is tightly associated with metabolic changes, which drive different immune subsets. Recent studies unveil the role of various metabolic enzymes in macrophage activation. Here, we show that [...] Read more.
Macrophages represent primary players of the innate immune system. Macrophage activation triggers several signaling pathways and is tightly associated with metabolic changes, which drive different immune subsets. Recent studies unveil the role of various metabolic enzymes in macrophage activation. Here, we show that malic enzyme 1 (ME1) is overexpressed in LPS-induced macrophages. Through chromatin immunoprecipitation, we demonstrate that ME1 transcriptional regulation is under control of NF-κB. Furthermore, ME1 activity is also increased in activated human PBMC-derived macrophages. Notably, ME1 gene silencing decreases nitric oxide as well as reactive oxygen species and prostaglandin E2 inflammatory mediators. Therefore, modulating ME1 provides a potential approach for immunometabolic regulation and in turn macrophage function. Full article
(This article belongs to the Special Issue Signaling Networks and Gene Expression in Immune Cells)
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14 pages, 3419 KiB  
Article
Immune Gene Networks from Lung Cancer Patients Treated with Immune Checkpoint Inhibitors
by Kyung Soo Kim, Taewon Kang and Dong Wook Jekarl
Biomedicines 2024, 12(3), 628; https://doi.org/10.3390/biomedicines12030628 - 12 Mar 2024
Viewed by 1283
Abstract
The association between immune checkpoint inhibitors (ICIs) and immune gene networks in squamous lung cancer (LUSC) and lung adenocarcinoma (LUAD) was studied. Immune gene networks were constructed using RNA-seq data from the gene expression omnibus (GEO) database. Datasets with more than 10 samples [...] Read more.
The association between immune checkpoint inhibitors (ICIs) and immune gene networks in squamous lung cancer (LUSC) and lung adenocarcinoma (LUAD) was studied. Immune gene networks were constructed using RNA-seq data from the gene expression omnibus (GEO) database. Datasets with more than 10 samples of normal control and tumor tissues were selected; of these, GSE87340, GSE120622, and GSE111907 were suitable for analysis. Gene set enrichment for pathway analysis was performed. For immune gene network construction, 998 unique immune genes were selected from 21 pathways in the Kyoto Encyclopedia of Genes and Genomes (KEGG). Gene function annotation was performed based on the KEGG, Gene Ontology, and Reactome databases. Tumor tissues showed decreased coagulation, hematopoiesis, and innate immune pathways, whereas complement- and coagulation-related genes were prominent in the tumor immune gene network. The average numbers of neighbors, clustering coefficients, network diameters, path lengths, densities, and heterogeneities were highest for normal tissue, followed by LUAD and LUSC. Decreased coagulation genes, which were prominent in tumor immune networks, imply functional attenuation. LUAD was deviated from normal tissue, based on network parameters. Tumor tissues showed decreased immune function, and the deviation of LUSC from normal tissue might explain LUSC’s better therapeutic response to ICI treatment. Full article
(This article belongs to the Special Issue Signaling Networks and Gene Expression in Immune Cells)
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Review

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24 pages, 1618 KiB  
Review
The Role of Immune Cells and Signaling Pathways in Diabetic Eye Disease: A Comprehensive Review
by Vincenzo Barone, Pier Luigi Surico, Francesco Cutrupi, Tommaso Mori, Gabriele Gallo Afflitto, Antonio Di Zazzo and Marco Coassin
Biomedicines 2024, 12(10), 2346; https://doi.org/10.3390/biomedicines12102346 - 15 Oct 2024
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Abstract
Diabetic eye disease (DED) encompasses a range of ocular complications arising from diabetes mellitus, including diabetic retinopathy, diabetic macular edema, diabetic keratopathy, diabetic cataract, and glaucoma. These conditions are leading causes of visual impairments and blindness, especially among working-age adults. Despite advancements in [...] Read more.
Diabetic eye disease (DED) encompasses a range of ocular complications arising from diabetes mellitus, including diabetic retinopathy, diabetic macular edema, diabetic keratopathy, diabetic cataract, and glaucoma. These conditions are leading causes of visual impairments and blindness, especially among working-age adults. Despite advancements in our understanding of DED, its underlying pathophysiological mechanisms remain incompletely understood. Chronic hyperglycemia, oxidative stress, inflammation, and neurodegeneration play central roles in the development and progression of DED, with immune-mediated processes increasingly recognized as key contributors. This review provides a comprehensive examination of the complex interactions between immune cells, inflammatory mediators, and signaling pathways implicated in the pathogenesis of DED. By delving in current research, this review aims to identify potential therapeutic targets, suggesting directions of research for future studies to address the immunopathological aspects of DED. Full article
(This article belongs to the Special Issue Signaling Networks and Gene Expression in Immune Cells)
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