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Cells
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Cellular and Molecular Determinants of Inflammation: Immune Cell Function, Immunometabolism...
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Cellular and Molecular Determinants of Inflammation: Immune Cell Function, Immunometabolism and Therapeutic Targeting

A Special Issue of Cells (ISSN 2073-4409) belonging to the section "Cellular Immunology".

Deadline for manuscript submissions: 15 February 2027 | Viewed by 2090

Editors

Dr. Zenith Khashim

E-Mail Website
Guest Editor
Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA
Interests: diabetes; pluripotent stem cells; immune cells; transplantation
Dr. Quinn P. Peterson

E-Mail Website
Guest Editor
Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA
Interests: pancreatic β-cells; stem cell; cell replacement therapy; diabetes; drug discovery

Special Issue Information

Dear Colleagues,

Inflammation is a fundamental biological process underlying the pathogenesis of numerous acute and chronic diseases; however, its regulation is governed by complex and interconnected cellular and molecular mechanisms that remain incompletely understood. Recent advances demonstrate that inflammatory responses are orchestrated through the coordinated actions of immune cells and non-immune cells, involving canonical immune signaling pathways, cell-intrinsic metabolic programs, organelle dynamics, and intercellular communication within tissue microenvironments. This Special Issue aims to provide a focused platform for studies offering mechanistic and functional insights into how immune cell function, immunometabolism, and cell-type-specific signaling pathways regulate inflammatory initiation, amplification, and resolution. Emphasis will be placed on mitochondrial and organelle-associated signaling, extracellular vesicle-mediated communication, and immune parenchymal cell crosstalk, including inflammatory processes relevant to transplantation, tissue injury, and immune tolerance, as well as metabolic tissues such as pancreatic β cells and stem cell-derived cellular models. We welcome original research articles and authoritative reviews that move beyond descriptive observations and establish causal relationships in inflammatory regulation. Contributions addressing inflammation in metabolic, autoimmune, cardiovascular, neuroinflammatory, and transplantation-associated diseases, as well as studies exploring therapeutic strategies to modulate immune-mediated inflammation, are especially encouraged.

Dr. Zenith Khashim
Dr. Quinn P. Peterson
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly 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

  • inflammation
  • immune regulation
  • immunometabolism
  • immune cell function
  • organelle signaling
  • mitochondrial dynamics
  • extracellular vesicles
  • intercellular communication
  • tissue microenvironment
  • immune tolerance

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Published Papers (2 papers)

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Research

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21 pages, 2501 KB  
Article
Platelet-Derived Exosome Product Prolongs Stem Cell-Derived β-Cell Graft Survival and Is Associated with Reduced Nk Cell Infiltration and Immunomodulation
by Zenith Khashim, Swikriti Shrestha, Shaimaa Hassoun, Ethan W. Law, Anna Marie R. Schornack, Jessica Lacap, Danielle J. Beetler, Gabriel J. Weigel, Lauren T. Jennings, Laura Becher, Chris Paradise, Atta Behfar, DeLisa Fairweather and Quinn P. Peterson
Cells 2026, 15(15), 1367; https://doi.org/10.3390/cells15151367 - 29 Jul 2026
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Abstract
Stem cell-derived β (SC-β) cells are a promising therapy for type 1 diabetes (T1D), but their long-term efficacy is limited by immune-mediated graft rejection. Platelet-derived exosome product (PEP) has emerged as a novel immunomodulatory agent, although its effect on SC-β cell xenograft rejection [...] Read more.
Stem cell-derived β (SC-β) cells are a promising therapy for type 1 diabetes (T1D), but their long-term efficacy is limited by immune-mediated graft rejection. Platelet-derived exosome product (PEP) has emerged as a novel immunomodulatory agent, although its effect on SC-β cell xenograft rejection remains unclear. Here, we evaluated PEP in stimulated human peripheral blood mononuclear cells (PBMCs) and in an immunocompetent mouse model of SC-β cell transplantation under the kidney capsule. Immune-related gene expression was assessed by quantitative PCR, immune cell infiltration by immunofluorescence, and graft function by circulating human insulin. In vitro, PEP reduced NK-cell-associated gene expression, including NK1.1, EOMES, and KLRK1, and increased IL-10 expression. In vivo, untreated SC-β cell xenografts showed progressive immune infiltration and loss of detectable human insulin by day 14, whereas PEP-treated grafts retained detectable insulin through day 14 across co-transplantation, pretreatment, and systemic administration strategies. PEP co-transplantation delayed, but did not prevent, xenograft rejection, with graft loss observed by day 21. This delay was associated with reduced NK1.1+ cell infiltration and lower expression of selected inflammatory and rejection-associated markers, including NK1.1, Nos2, and Nlrp3. These findings suggest that PEP modulates graft-associated immune responses and may serve as an adjunct immunomodulatory strategy for stem cell-based therapies for type 1 diabetes. Further studies are needed to evaluate sustained graft durability, safety, and translational efficacy. Full article
(This article belongs to the Special Issue Cellular and Molecular Determinants of Inflammation: Immune Cell Function, Immunometabolism and Therapeutic Targeting)
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Review

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18 pages, 720 KB  
Review
Interleukin-17 in Health and Disease: Special Focus on Its Role in Autoimmune Hepatitis
by Ştefan Agoston, Alina Grama, Alexia Onaciu, Alexandra Mititelu, Gabriel Benţa and Tudor Lucian Pop
Cells 2026, 15(10), 915; https://doi.org/10.3390/cells15100915 - 17 May 2026
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Abstract
Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease characterized by hypergammaglobulinemia, circulating antibodies, and distinctive histological features, with a higher prevalence in females. Immune responses targeting hepatic antigens are considered the main mechanism behind AIH. Many cytokines are involved in the inflammatory [...] Read more.
Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease characterized by hypergammaglobulinemia, circulating antibodies, and distinctive histological features, with a higher prevalence in females. Immune responses targeting hepatic antigens are considered the main mechanism behind AIH. Many cytokines are involved in the inflammatory response typical of this disease. Interleukin 17 (IL-17) is a powerful pro-inflammatory protein that serves as a key link between the innate and adaptive immune systems. It plays an important role in regulating the inflammatory response in various tissues, including the liver. Several studies have shown that increased IL-17 levels are associated with the severity and progression of AIH. This review explores IL-17’s role in the AIH inflammatory pathway and summarizes existing evidence linking it to liver damage. We also highlight the potential of future therapies targeting this cytokine. Full article
(This article belongs to the Special Issue Cellular and Molecular Determinants of Inflammation: Immune Cell Function, Immunometabolism and Therapeutic Targeting)
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