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Regulation and Activation of Immune Cells through the Mitochondria
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Regulation and Activation of Immune Cells through the Mitochondria

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: 20 May 2025 | Viewed by 3624

Special Issue Editor

Dr. Špela Konjar

E-Mail Website
Guest Editor
Center of Proteomics, Medical Faculty, University of Rijeka, Ul. Braće Branchetta 20, 51000 Rijeka, Croatia
Interests: immunometabolism of T cells; T cells at the epithelial barrier; activation of T-cell system biology

Special Issue Information

Dear Colleagues,

Following the discovery of the Krebs cycle in the 1950s, mitochondria were primarily linked to cellular bioenergetics. However, in the 1990s, a shift in perspective occurred as research demonstrated mitochondria significant involvement in apoptotic cell death. These findings paved the way to the idea that these organelles have a role in cell signaling, as now confirmed by many publications. Consequently, mitochondria have been implicated in numerous intricate cellular processes extending beyond cell death, including autophagy, stem cell differentiation, and the regulation of immune responses such as activation.

Activation of immune cells, as one of the key regulation processes of immune cells, is critically dependent on specific metabolic programs with mitochondria involvement. Upon activation by a virus, bacteria or their products, immune cells undergo dramatic metabolic changes, dictated by mitochondria, including the generation of ATP from the oxidation of nutrients and supplying precursors for the synthesis of macromolecules and post-translational modifications. This can cause changes in several metabolic pathways such as the tricarboxylic acid (TCA) cycle and amino acid and lipid metabolism, leading to the accumulation of certain metabolites. When activated, T cells swiftly undergo proliferation and intensify gene transcription-translation processes to support essential immune responses, including the production of cytokines and adhesion molecules. Consequently, they must enhance their protein synthesis. Based on the activation state of various immune cells, including T cells, macrophages, and mast cells, mitochondria have been observed to undergo specific changes in their structural configurations, such as fusion or fission. All these alterations in metabolism of mitochondria aid the cells in combating invading pathogens, both through direct and indirect mechanisms.

This Special Issue is focused on the understanding regulation of different immune cells through mitochondria, how regulation of immune cells is impacting mitochondrial dynamics, biogenesis, mitophagy…. Additionally, how dysregulation of immune cells such as different forms of inflammation are affecting mitochondria phenotype in immune cells. Research papers, review, short communication, perspective articles exploring mitochondria and immune cells are welcome.

Dr. Špela Konjar
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

  • mitophagy in immune cells
  • autophagy and mitochondria in immune cells
  • fission and fusion of mitochondria in immune cells
  • oxphos and mitochondria in immune cells
  • glycolysis and mitochondria in immune cells
  • tissue residency of immune cells and their mitochondria
  • tumor infiltrating lymphocytes and their mitochondria
  • mitochondria in inflammation

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Published Papers (2 papers)

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13 pages, 3047 KiB  
Article
Inhibition of the CXCR4/PLC Signaling Increases Dexamethasone-Induced Sensitivity by Activating the Mitochondrial Apoptotic Pathway in B-Cell Acute Lymphoblastic Leukemia
by Souleymane Abdoul-Azize, Jean-Pierre Vannier and Pascale Schneider
Int. J. Mol. Sci. 2025, 26(8), 3489; https://doi.org/10.3390/ijms26083489 - 8 Apr 2025
Viewed by 289
Abstract
Understanding the mechanisms underlying glucocorticoid (GC) resistance in B-cell acute lymphoblastic leukemia (B-ALL) is essential to improve survival rates in relapsed children. We previously showed that GCs paradoxically induced their own resistance in B-ALL through CXCR4/PLC signaling, and that the inhibition of this [...] Read more.
Understanding the mechanisms underlying glucocorticoid (GC) resistance in B-cell acute lymphoblastic leukemia (B-ALL) is essential to improve survival rates in relapsed children. We previously showed that GCs paradoxically induced their own resistance in B-ALL through CXCR4/PLC signaling, and that the inhibition of this pathway significantly reverses GC resistance in B-ALL cells and improves survival of GC-treated NSG mice in vivo. Here, we sought to determine whether the enhancement of GC sensitivity via inhibition of the CXCR4/PLC axis is associated with disruption of the mitochondrial pathway. Analysis of our previous transcriptomic data revealed that in B-ALL, the PLC inhibitor U73122 compromised multiple metabolic pathways related to metabolic reprogramming, mitochondrial function, and oxidative stress. Inhibition of PLC with U73122, protein kinase C with GF109203X, or CXCR4 with AMD3100 significantly potentiated dexamethasone (Dex)-induced mitochondrial membrane potential depolarization, reactive oxygen species production, cytochrome c release, caspase-3 activation, and decreased O2 consumption in B-ALL cells. These observations were also confirmed after Dex treatment in a B-ALL Nalm-6 cell line transfected with CXCR4 small interfering RNA. Moreover, co-treatment with Dex and CXCR4, PKC, or PLC inhibitors increased the levels of the pro-apoptotic protein BIM (BCL-2 interacting mediator of cell death) and, consequently, promoted the cell death process. Together, these findings suggest that the CXCR4/PLC axis reduces Dex efficacy by limiting mitochondrial apoptotic activity. Full article
(This article belongs to the Special Issue Regulation and Activation of Immune Cells through the Mitochondria)
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22 pages, 2823 KiB  
Article
Physiologically Achievable Concentration of 2-Deoxy-D-Glucose Stimulates IFN-γ Secretion in Activated T Cells In Vitro
by Jernej Repas, Tjaša Frlic, Tadeja Snedec, Andreja Nataša Kopitar, Harald Sourij, Andrej Janež and Mojca Pavlin
Int. J. Mol. Sci. 2024, 25(19), 10384; https://doi.org/10.3390/ijms251910384 - 26 Sep 2024
Viewed by 2006
Abstract
2-deoxy-D-glucose (2DG) is a glycolysis and protein N-glycosylation inhibitor with promising anti-tumor and immunomodulatory effects. However, 2DG can also suppress T cell function, including IFN-γ secretion. Few human T cell studies have studied low-dose 2DG, which can increase IFN-γ in a Jurkat clone. [...] Read more.
2-deoxy-D-glucose (2DG) is a glycolysis and protein N-glycosylation inhibitor with promising anti-tumor and immunomodulatory effects. However, 2DG can also suppress T cell function, including IFN-γ secretion. Few human T cell studies have studied low-dose 2DG, which can increase IFN-γ in a Jurkat clone. We therefore investigated 2DG’s effect on IFN-γ in activated human T cells from PBMCs, with 2DG treatment commenced either concurrently with activation or 48 h after activation. Concurrent 2DG treatment decreased IFN-γ secretion in a dose-dependent manner. However, 2DG treatment of pre-activated T cells had a hormetic effect on IFN-γ, with 0.15–0.6 mM 2DG (achievable in vivo) increasing and >2.4 mM 2DG reducing its secretion. In contrast, IL-2 levels declined monotonously with increasing 2DG concentration. Lower 2DG concentrations reduced PD-1 and increased CD69 expression regardless of treatment timing. The absence of increased T-bet or Eomes expression or IFNG transcription suggests another downstream mechanism. 2DG dose-dependently induced the unfolded protein response, suggesting a possible role in increased IFN-γ secretion, possibly by increasing the ER folding capacity for IFN-γ via increased chaperone expression. Overall, low-dose, short-term 2DG exposure could potentially improve the T cell anti-tumor response. Full article
(This article belongs to the Special Issue Regulation and Activation of Immune Cells through the Mitochondria)
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