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10.5
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Cells
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Immune Cell Effect on the Endothelium
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Immune Cell Effect on the Endothelium

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 9690

Special Issue Editors

Dr. Constantinos Mikelis

E-Mail Website1 Website2
Guest Editor
Department of Pharmacy, University of Patras, 26504 Rion, Greece
Interests: vascular physiology; endothelial cells; angiogenesis; permeability; metastasis
Special Issues, Collections and Topics in MDPI journals
Dr. Margarita Lamprou

E-Mail Website
Guest Editor
Department of Pharmacy, University of Patras, 26504 Rion, Greece
Interests: bone angiogenesis; endothelial cells; permeability; metastasis

Special Issue Information

Dear Colleagues,

Cell-to-cell communication among diverse cell types plays a vital role in tissue and organism homeostasis. At the same time, dysregulated intercellular communication shapes the pathophysiology of multiple diseases. The endothelial cells participate in the pathophysiology of inflammatory disorders, including cancer, and their behavior is regulated by different cell types, such as immune cells, fibroblasts and tumor cells in the case of malignancies. This Special Issue focuses on the reciprocal interaction between immune and endothelial cells; the means of this interaction, such as cytokines or extracellular vesicles; the molecular mechanisms; and its effect on vascular physiology or pathophysiology and the characteristic of inflammatory diseases.

Dr. Constantinos Mikelis
Dr. Margarita Lamprou
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 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-blind 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

  • immune cells
  • endothelial cells
  • cytokines
  • extracellular vesicles
  • angiogenesis
  • vascular permeability

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Published Papers (3 papers)

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Research

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22 pages, 8835 KB  
Article
High-Frequency Irreversible Electroporation Alters Proteomic Profiles and Tropism of Small Tumor-Derived Extracellular Vesicles to Promote Immune Cell Infiltration
by Kelsey R. Murphy, Kenneth N. Aycock, Spencer Marsh, Liping Yang, Jonathan Hinckley, Aubrie Selmek, Robert Gourdie, Shay Bracha, Rafael V. Davalos, John H. Rossmeisl and Nikolaos G. Dervisis
Cells 2025, 14(22), 1782; https://doi.org/10.3390/cells14221782 - 13 Nov 2025
Viewed by 1104
Abstract
High-frequency irreversible electroporation (H-FIRE) is a nonthermal tumor ablation technique that disrupts the blood–brain barrier (BBB) in a focal and reversible manner. However, the mechanisms underlying this disruption remain poorly understood, particularly the role of small tumor-derived extracellular vesicles (sTDEVs) released from ablated [...] Read more.
High-frequency irreversible electroporation (H-FIRE) is a nonthermal tumor ablation technique that disrupts the blood–brain barrier (BBB) in a focal and reversible manner. However, the mechanisms underlying this disruption remain poorly understood, particularly the role of small tumor-derived extracellular vesicles (sTDEVs) released from ablated tumor cells. In this study, we investigate the proteomic and functional alterations of sTDEVs released from F98 glioma and LL/2 Lewis lung carcinoma cells following H-FIRE ablation. Mass spectrometry analysis revealed 108 unique proteins in sTDEVs derived from ablative doses of H-FIRE, which are capable of disrupting the BBB in an in vitro model. Proteomic analysis of TDEVs highlights key changes in pathways related to integrin signaling, Platelet-derived growth factor receptor (PDGFR) signaling, and ubiquitination, which may underline their interactions with brain endothelial cells. These “disruptive” sTDEVs exhibit enhanced tropism for cerebral endothelial cells both in vitro and in vivo, where they persist in the brain longer than sTDEVs released after non-ablative H-FIRE doses. Notably, when introduced into a healthy Fischer rat model, disruptive sTDEVs are associated with increased recruitment of Iba1+ immune cells, suggesting a potential role in modulating post-ablation immune responses. However, despite their altered protein composition, these vesicles do not directly increase BBB permeability in vivo. This study is the first to demonstrate that electroporation-based tumor ablation significantly alters the composition and functionality of tumor-derived extracellular vesicles, potentially influencing the tumor microenvironment post-ablation. These findings have important implications for developing multimodal treatment strategies that combine H-FIRE with systemic therapies to enhance efficacy while managing the peritumoral microenvironment. Full article
(This article belongs to the Special Issue Immune Cell Effect on the Endothelium)
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Review

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27 pages, 2018 KB  
Review
Dysregulation of Neutrophil–Endothelial Communication in Sepsis: Mechanisms and Therapeutic Perspectives
by Nazgol Esmalian Afyouni, Mohammad F. Kiani and Laurie E. Kilpatrick
Cells 2026, 15(7), 581; https://doi.org/10.3390/cells15070581 - 25 Mar 2026
Viewed by 790
Abstract
Sepsis is a clinical syndrome defined as life-threatening organ dysfunction caused by a dysregulation in immune response to infection. Dysregulated neutrophil activity plays a critical role in sepsis-induced organ failure through interactions with the vascular endothelial cells during forward and reverse migration, resulting [...] Read more.
Sepsis is a clinical syndrome defined as life-threatening organ dysfunction caused by a dysregulation in immune response to infection. Dysregulated neutrophil activity plays a critical role in sepsis-induced organ failure through interactions with the vascular endothelial cells during forward and reverse migration, resulting in vascular barrier disruption and increased neutrophil trafficking into vital organs. Therapeutic approaches for treating sepsis are mainly supportive. Due to limited clinical translation from rodent models, complexity of the pathophysiology, and most importantly, the heterogenous nature of sepsis, no significant therapeutics have been successfully developed to address the underlying immune dysregulation. In this review, we will discuss the important gap in knowledge on the fundamental mechanisms of neutrophil–endothelial interaction, the role that neutrophil forward and reverse migration plays in organ damage in sepsis, and how neutrophil and endothelial cell heterogeneity impact cell–cell communication. We will explore emerging methodologies, including novel omic and microphysiological systems, to study the underlying mechanism of neutrophil–endothelial interaction and neutrophil forward migration/reverse migration. Finally, we will review potential therapeutic targets modulating neutrophil–endothelial interaction and the challenges of translating them from bench to bedside. Full article
(This article belongs to the Special Issue Immune Cell Effect on the Endothelium)
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18 pages, 1566 KB  
Review
The Role of Soluble CD163 (sCD163) in Human Physiology and Pathophysiology
by Andriana Plevriti, Margarita Lamprou, Eleni Mourkogianni, Nikolaos Skoulas, Maria Giannakopoulou, Md Sanaullah Sajib, Zhiyong Wang, George Mattheolabakis, Antonios Chatzigeorgiou, Antonia Marazioti and Constantinos M. Mikelis
Cells 2024, 13(20), 1679; https://doi.org/10.3390/cells13201679 - 11 Oct 2024
Cited by 30 | Viewed by 7265
Abstract
Soluble CD163 (sCD163) is a circulating inflammatory mediator, indicative of acute and chronic, systemic and non-systemic inflammatory conditions. It is the cleavage outcome, consisting of almost the entire extracellular domain, of the CD163, a receptor expressed in monocytic lineages. Its expression is proportional [...] Read more.
Soluble CD163 (sCD163) is a circulating inflammatory mediator, indicative of acute and chronic, systemic and non-systemic inflammatory conditions. It is the cleavage outcome, consisting of almost the entire extracellular domain, of the CD163, a receptor expressed in monocytic lineages. Its expression is proportional to the abundance of CD163+ macrophages. Various mechanisms trigger the shedding of the CD163 receptor or the accumulation of CD163-expressing macrophages, inducing the sCD163 concentration in the circulation and bodily fluids. The activities of sCD163 range from hemoglobin (Hb) scavenging, macrophage marker, decoy receptor for cytokines, participation in immune defense mechanisms, and paracrine effects in various tissues, including the endothelium. It is an established marker of macrophage activation and thus participates in many diseases, including chronic inflammatory conditions, such as atherosclerosis, asthma, and rheumatoid arthritis; acute inflammatory conditions, such as sepsis, hepatitis, and malaria; insulin resistance; diabetes; and tumors. The sCD163 levels have been correlated with the severity, stage of the disease, and clinical outcome for many of these conditions. This review article summarizes the expression and role of sCD163 and its precursor protein, CD163, outlines the sCD163 generation mechanisms, the biological activities, and the known underlying molecular mechanisms, with an emphasis on its impact on the endothelium and its contribution in the pathophysiology of human diseases. Full article
(This article belongs to the Special Issue Immune Cell Effect on the Endothelium)
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