ijms-logo

Journal Browser

Journal Browser

Immune Cell Signaling and Immune Metabolism in Inflammatory Processes

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 2023) | Viewed by 1664

Special Issue Editors


E-Mail Website
Guest Editor
Health Campus Immunology, Infectiology, and Inflammation, Institute of Molecular and Clinical Immunology, Otto-von-Guericke University, Leipziger Str. 44, D-39120 Magdeburg, Germany
Interests: lymphocyte signaling; T-cell receptor signaling; Zap70; Lck; tyrosine kinases; T-cell activation; thymic development; natural products; immunomodulation
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Otto-von-Guericke-University Magdeburg, 39120 Magdeburg, Germany
Interests: immunology; microbiology; T cells, T cell signaling; calcium; innate immune system; host-pathogen interaction; ion channels in immunity; CAR T cells; immune cell therapy; immunometabolism

Special Issue Information

Dear Colleagues,

Over the past few years it has become evident that immune cell signaling regulates the energy metabolism of adaptive as well as innate immune cells. In T cells, antigen recognition by the T-cell receptor (TCR) results in the activation of different transcription factors regulating the expression of genes encoding for key metabolic enzymes. Similarly, signaling via non-adaptive sensing receptors such as Toll-like receptors (TLRs) stimulate metabolic reprogramming in innate immune cells. It has also become evident that the energy metabolism affects several immune cell functions and hence, it plays an essential role in the regulation of immune responses. Thus, the better understanding of how signaling processes regulate metabolic pathways in adaptive and innate immune cells will provide new avenues for the development of new therapeutic approaches to modulate immune responses and to ameliorate inflammatory diseases.

The Special Issue “Immune Cell Signaling and Immune Metabolism in Inflammatory Processes” welcomes original research and review articles with a particular focus on the interconnection of immune cell signaling and immunometabolism during inflammation.

Prof. Dr. Luca Simeoni
Prof. Dr. Sascha Kahlfuss
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. 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

  • immune cell signaling
  • signal transduction
  • T cell receptor
  • adaptive and innate immune cells
  • immune cells
  • gene expression
  • epigenetics
  • inflammation

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

19 pages, 6850 KiB  
Article
Epithelial Galectin-3 Induced the Mitochondrial Complex Inhibition and Cell Cycle Arrest of CD8+ T Cells in Severe/Critical COVID-19
by Yudie Wang, Cheng Yang, Zhongyi Wang, Yi Wang, Qing Yan, Ying Feng, Yanping Liu, Juan Huang and Jingjiao Zhou
Int. J. Mol. Sci. 2023, 24(16), 12780; https://doi.org/10.3390/ijms241612780 - 14 Aug 2023
Cited by 1 | Viewed by 1440
Abstract
Previous research suggested that the dramatical decrease in CD8+ T cells is a contributing factor in the poor prognosis and disease progression of COVID-19 patients. However, the underlying mechanisms are not fully understood. In this study, we conducted Single-cell RNA sequencing (scRNA-seq) [...] Read more.
Previous research suggested that the dramatical decrease in CD8+ T cells is a contributing factor in the poor prognosis and disease progression of COVID-19 patients. However, the underlying mechanisms are not fully understood. In this study, we conducted Single-cell RNA sequencing (scRNA-seq) and single-cell T cell receptor sequencing (scTCR-seq) analysis, which revealed a proliferative-exhausted MCM+FASLGlow CD8+ T cell phenotype in severe/critical COVID-19 patients. These CD8+ T cells were characterized by G2/M cell cycle arrest, downregulation of respiratory chain complex genes, and inhibition of mitochondrial biogenesis. CellChat analysis of infected lung epithelial cells and CD8+ T cells found that the galectin signaling pathway played a crucial role in CD8+ T cell reduction and dysfunction. To further elucidate the mechanisms, we established SARS-CoV-2 ORF3a-transfected A549 cells, and co-cultured them with CD8+ T cells for ex vivo experiments. Our results showed that epithelial galectin-3 inhibited the transcription of the mitochondrial respiratory chain complex III/IV genes of CD8+ T cells by suppressing the nuclear translocation of nuclear respiratory factor 1 (NRF1). Further findings showed that the suppression of NRF1 translocation was associated with ERK-related and Akt-related signaling pathways. Importantly, the galectin-3 inhibitor, TD-139, promoted nuclear translocation of NRF1, thus enhancing the expression of the mitochondrial respiratory chain complex III/IV genes and the mitochondrial biogenesis of CD8+ T cells. Our study provided new insights into the immunopathogenesis of COVID-19 and identified potential therapeutic targets for the prevention and treatment of severe/critical COVID-19 patients. Full article
(This article belongs to the Special Issue Immune Cell Signaling and Immune Metabolism in Inflammatory Processes)
Show Figures

Figure 1

Back to TopTop