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Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers

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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 June 2025 | Viewed by 16515

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Dr. Evgeny E. Bezsonov

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1. Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
2. Laboratory of Cellular and Molecular Pathology of Cardiovascular System, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution “Petrovsky National Research Center of Surgery”, 117418 Moscow, Russia
3. Department of Biology and General Genetics, I.M. Sechenov First Moscow State Medical University (Sechenov University), 105043 Moscow, Russia
Interests: atherosclerosis; mitophagy; atherogenicity; atherosclerosis; autoantibodies; inflammation; innate immunity; amyloid
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Dear Colleagues,

Despite recent progress in treatment of atherosclerosis related to lipid-lowering therapies still we are very far from being able to completely eliminate or prevent this pathological condition. The main reason of this problem is the lack of complete understanding of all pathological changes happening upon atherosclerosis development which makes almost impossible the creation of new effective drugs. It should be mentioned also that chronic inflammation is believed to be one of the main contributing factors for the development of plethora of diseases starting from atherosclerosis, cancer, rheumatoid arthritis and ending with inevitable aging process.

The Special Issue will be dedicated to the role of immune cells in the development of atherosclerosis and other non-infectious inflammatory diseases. The aim of this Special Issue is to try to take a new look at the inflammatory component of atherosclerosis development including the comparison of the role of immune cells in inflammation in atherosclerosis and in other non-infectious inflammatory diseases with the ultimate goal to find general principles and targets for therapy and drug creation.

All studies devoted to the role of immunity-related cells (such as macrophages, T- and B- cells etc.) in pathological mechanisms non-infectious inflammatory diseases development will be welcome for the submission.

Dr. Evgeny E. Bezsonov
Guest Editor

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Keywords

cytokines
immunity cells
atherosclerosis
inflammation
immunity

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13 pages, 3589 KiB

Open AccessArticle

Integrated Analysis of Phagocytic and Immunomodulatory Markers in Cervical Cancer Reveals Constellations of Potential Prognostic Relevance

by Angel Yordanov, Polina Damyanova, Mariela Vasileva-Slaveva, Ihsan Hasan, Stoyan Kostov and Velizar Shivarov

Int. J. Mol. Sci. 2024, 25(16), 9117; https://doi.org/10.3390/ijms25169117 - 22 Aug 2024

Viewed by 879

Abstract

Despite improvements in vaccination, screening, and treatment, cervical cancer (CC) remains a major healthcare problem on a global scale. The tumor microenvironment (TME) plays an important and controversial role in cancer development, and the mechanism of the tumor’s escape from immunological surveillance is still not clearly defined. We aim to investigate the expression of CD68 and CD47 in patients with different histological variants of CC, tumor characteristics, and burden. This is a retrospective cohort study performed on paraffin-embedded tumor tissues from 191 patients diagnosed with CC between 2014 and 2021 at the Medical University Pleven, Bulgaria. Slides for immunohistochemical (IHC) evaluation were obtained, and the expression of CD68 was scored in intratumoral (IT) and stromal (ST) macrophages (CD68+cells) using a three-point scoring scale. The CD47 expression was reported as an H-score. All statistical analyses were performed using R v. 4.3.1 for Windows. Infiltration by CD68-IT cells in the tumor depended on histological type and the expression of CD47. Higher levels of the CD47 H-score were significantly more frequent among patients in the early stage. Higher levels of infiltration by CD68-ST cells were associated with worse prognosis, and the infiltration of CD68-IT cells was associated with reduced risk of death from neoplastic disease. TME is a complex ecosystem that has a major role in the growth and development of tumors. Macrophages are a major component of innate immunity and, when associated with a tumor process, are defined as TAM. Tumor cells try to escape immunological surveillance in three ways, and one of them is reducing immunogenicity by the overexpression of negative coreceptors by T-lymphocytes and their ligands on the surface of tumor cells. One such mechanism is the expression of CD47 in tumor cells, which sends a “don’t eat me” signal to the macrophages and, thus, prevents phagocytosis. To our knowledge, this is the first study that has tried to establish the relationship between the CD47 and CD68 expression levels and some clinicopathologic features in CC. We found that the only clinicopathological feature implicating the level of CD68 infiltration was the histological variant of the tumor, and only for CD68-IT–high levels were these observed in SCC. High levels of CD47 expression were seen more frequently in pT1B than pT2A and pT2B in the FIGO I stage than in the FIGO II and III stages. Infiltration by large numbers of CD68-IT cells was much more common among patients with a high expression of CD47 in tumor cells. A high level of infiltration by CD68-ST cells was associated with a worse prognosis, and a high level of infiltration by CD68-ST cells was associated with a lower risk of death from cancer. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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28 pages, 12614 KiB

Open AccessArticle

Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance

by Dzhuliia Dzhalilova, Maria Silina, Ivan Tsvetkov, Anna Kosyreva, Natalia Zolotova, Elena Gantsova, Vladimir Kirillov, Nikolay Fokichev and Olga Makarova

Int. J. Mol. Sci. 2024, 25(14), 7801; https://doi.org/10.3390/ijms25147801 - 16 Jul 2024

Viewed by 1118

Abstract

One of the factors contributing to colorectal cancer (CRC) development is inflammation, which is mostly hypoxia-associated. This study aimed to characterize the morphological and molecular biological features of colon tumors in mice that were tolerant and susceptible to hypoxia based on colitis-associated CRC (CAC). Hypoxia tolerance was assessed through a gasping time evaluation in a decompression chamber. One month later, the animals were experimentally modeled for colitis-associated CRC by intraperitoneal azoxymethane administration and three dextran sulfate sodium consumption cycles. The incidence of tumor development in the distal colon in the susceptible to hypoxia mice was two times higher and all tumors (100%) were represented by adenocarcinomas, while in the tolerant mice, only 14% were adenocarcinomas and 86% were glandular intraepithelial neoplasia. The tumor area assessed on serially stepped sections was statistically significantly higher in the susceptible animals. The number of macrophages, CD3−CD19+, CD3+CD4+, and NK cells in tumors did not differ between animals; however, the number of CD3+CD8+ and vimentin+ cells was higher in the susceptible mice. Changes in the expression of genes regulating the response to hypoxia, inflammation, cell cycle, apoptosis, and epithelial barrier functioning in tumors and the peritumoral area depended on the initial mouse’s hypoxia tolerance, which should be taken into account for new CAC diagnostics and treatment approaches development. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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19 pages, 6626 KiB

Open AccessArticle

Engineered CD147-Deficient THP-1 Impairs Monocytic Myeloid-Derived Suppressor Cell Differentiation but Maintains Antibody-Dependent Cellular Phagocytosis Function for Jurkat T-ALL Cells with Humanized Anti-CD147 Antibody

by Thanathat Pamonsupornwichit, Kanokporn Sornsuwan, On-anong Juntit, Umpa Yasamut, Nuchjira Takheaw, Watchara Kasinrerk, Phenphichar Wanachantararak, Kanchanok Kodchakorn, Piyarat Nimmanpipug, Nutjeera Intasai and Chatchai Tayapiwatana

Int. J. Mol. Sci. 2024, 25(12), 6626; https://doi.org/10.3390/ijms25126626 - 16 Jun 2024

Cited by 1 | Viewed by 1644

Abstract

CD147 is upregulated in cancers, including aggressive T-ALL. Traditional treatments for T-ALL often entail severe side effects and the risk of relapse, highlighting the need for more efficacious therapies. ADCP contributes to the antitumor response by enhancing the ability of phagocytic cells to engulf cancer cells upon antibody binding. We aimed to engineer CD147^KO THP-1 cells and evaluated their differentiation properties compared to the wild type. A humanized anti-CD147 antibody, HuM6-1B9, was also constructed for investing the phagocytic function of CD147^KO THP-1 cells mediated by HuM6-1B9 in the phagocytosis of Jurkat T cells. The CD147^KO THP-1 was generated by CRISPR/Cas9 and maintained polarization profiles. HuM6-1B9 was produced in CHO-K1 cells and effectively bound to CD147 with high binding affinity (K_D: 2.05 ± 0.30 × 10⁻⁹ M). Additionally, HuM6-1B9 enhanced the phagocytosis of Jurkat T cells by CD147^KO THP-1-derived LPS-activated macrophages (M-LPS), without self-ADCP. The formation of THP-1-derived mMDSC was limited in CD147^KO THP-1 cells, highlighting the significant impact of CD147 deletion. Maintaining expression markers and phagocytic function in CD147^KO THP-1 macrophages supports future engineering and the application of induced pluripotent stem cell-derived macrophages. The combination of HuM6-1B9 and CD147^KO monocyte-derived macrophages holds promise as an alternative strategy for T-ALL. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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13 pages, 2603 KiB

Open AccessArticle

Analysis of Immune Cell Subsets in Peripheral Blood from Patients with Engineered Stone Silica-Induced Lung Inflammation

by Gema Jiménez-Gómez, Antonio Campos-Caro, Alejandro García-Núñez, Alberto Gallardo-García, Antonio Molina-Hidalgo and Antonio León-Jiménez

Int. J. Mol. Sci. 2024, 25(11), 5722; https://doi.org/10.3390/ijms25115722 - 24 May 2024

Viewed by 826

Abstract

Silicosis caused by engineered stone (ES-silicosis) is an emerging worldwide issue characterized by inflammation and fibrosis in the lungs. To our knowledge, only a few reports have investigated leukocyte/lymphocyte subsets in ES-silicosis patients. The present study was designed to explore the proportions of the main lymphocyte subsets in ES-silicosis patients stratified into two groups, one with simple silicosis (SS) and the other with a more advanced state of the disease, defined as progressive massive fibrosis (PMF). The proportions of B (memory and plasmablasts) cells, T (helper, cytotoxic, regulatory) cells, and natural killer (NK) (regulatory and cytotoxic) cells were investigated by multiparameter flow cytometry in 91 ES-silicosis patients (53 SS patients and 38 PMF patients) and 22 healthy controls (HC). Although the total number of leukocytes did not differ between the groups studied, lymphopenia was observed in patients compared to healthy controls. Compared with those in healthy controls, the proportions of memory B cells, naïve helper T cells, and the CD4⁺/CD8⁺ T cells’ ratio in the peripheral blood of patients with silicosis were significantly decreased, while the percentages of plasma cells, memory helper T cells, and regulatory T cells were significantly increased. For the NK cell subsets, no significant differences were found between the groups studied. These results revealed altered cellular immune processes in the peripheral blood of patients with ES-silicosis and provided further insight into silicosis pathogenesis. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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16 pages, 6502 KiB

Open AccessArticle

Immunological Landscapes in Lung Transplantation: Insights from T Cell Profiling in BAL and PBMC

by Tharushi Ayanthika de Silva, Simon Apte, Joanne Voisey, Kirsten Spann, Maxine Tan, Daniel Chambers and Brendan O’Sullivan

Int. J. Mol. Sci. 2024, 25(5), 2476; https://doi.org/10.3390/ijms25052476 - 20 Feb 2024

Viewed by 1464

Abstract

Lung transplant recipients frequently encounter immune-related complications, including chronic lung allograft dysfunction (CLAD). Monitoring immune cells within the lung microenvironment is pivotal for optimizing post-transplant outcomes. This study examined the proportion of T cell subsets in paired bronchoalveolar lavage (BAL) and peripheral PBMC comparing healthy (n = 4) and lung transplantation patients (n = 6, no CLAD and n = 14 CLAD) using 14-color flow cytometry. CD4+ T cell proportions were reduced in CD3 cells in both PBMC and BAL, and positive correlations were discerned between T cell populations in peripheral PBMC and BAL, suggesting the prospect of employing less invasive PBMC sampling as a means of monitoring lung T cells. Furthermore, regulatory T cells (Tregs) were enriched in BAL when compared to peripheral PBMC for transplant recipients. A parallel positive correlation emerged between Treg proportions in BAL and peripheral PBMC, underscoring potential avenues for monitoring lung Tregs. Finally, the most promising biomarker was the Teff (CD8+Granzyme B+)–Treg ratio, which was higher in both the PBMC and BAL of transplant recipients compared to healthy individuals, and increased in the patients with CLAD compared to no CLAD and healthy patients. Conclusions: Distinct T cell profiles in BAL and peripheral PBMC underscore the significance of localized immune monitoring in lung transplantation. The Teff (CD8+granzyme B+)–Treg ratio, particularly within the context of CLAD, emerges as a promising blood and BAL biomarker reflective of inflammation and transplant-related complications. These findings emphasize the imperative need for personalized immune monitoring strategies that tailored to address the unique immunological milieu in post-transplant lungs. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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22 pages, 8967 KiB

Open AccessArticle

Traversing through the Mechanistic Event Analysis in IL-6 and IL-17 Signaling for a New Therapeutic Paradigm in NSCLC

by Riya Khilwani and Shailza Singh

Int. J. Mol. Sci. 2024, 25(2), 1216; https://doi.org/10.3390/ijms25021216 - 19 Jan 2024

Cited by 2 | Viewed by 1662

Abstract

IL-6 and IL-17 are paradoxical cytokines that progress inflammatory states in chronic diseases, including cancer. In lung cancer, their role has been elucidated to favor cancer development by modulating signaling mechanisms critical to cellular growth. The intrinsic ability of these cytokines to influence macroautophagy is yet another reason to facilitate lung cancer. Here, we employed a systems immunology approach to discover the mechanistic role of these cytokines in cancer development. In a biological system, at later stages, the activation of NFkB stimulates immunosuppressive phenotypes to achieve tolerating effects in a transformed cell. We found that the upregulation of cytokines signaled M2 macrophages to modulate tumor responses through the activation of autophagic intermediates and inflammasome mediators. This caused immune perturbations in the tumor microenvironment, which were associated with cancer inflammation. To address these inflammatory states, we performed triggered event analysis to examine whether overexpressing immune effectors or downregulating immune suppressors may have an effect on cancer reversal. Interestingly, the inhibition of immune regulators opposed the model outcome to an increased immune response. Therefore, IL6-IL17-mediated regulation of lung cancer may address tumor malignancy and potentiate the development of newer therapeutics for NSCLC. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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Review

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16 pages, 902 KiB

Open AccessReview

The Role of CD4⁺T Cells in Nonalcoholic Steatohepatitis and Hepatocellular Carcinoma

by Yadi Miao, Ziyong Li, Juan Feng, Xia Lei, Juanjuan Shan, Cheng Qian and Jiatao Li

Int. J. Mol. Sci. 2024, 25(13), 6895; https://doi.org/10.3390/ijms25136895 - 23 Jun 2024

Viewed by 1799

Abstract

Hepatocellular carcinoma (HCC) has become the fourth leading cause of cancer-related deaths worldwide; annually, approximately 830,000 deaths related to liver cancer are diagnosed globally. Since early-stage HCC is clinically asymptomatic, traditional treatment modalities, including surgical ablation, are usually not applicable or result in recurrence. Immunotherapy, particularly immune checkpoint blockade (ICB), provides new hope for cancer therapy; however, immune evasion mechanisms counteract its efficiency. In addition to viral exposure and alcohol addiction, nonalcoholic steatohepatitis (NASH) has become a major cause of HCC. Owing to NASH-related aberrant T cell activation causing tissue damage that leads to impaired immune surveillance, NASH-associated HCC patients respond much less efficiently to ICB treatment than do patients with other etiologies. In addition, abnormal inflammation contributes to NASH progression and NASH–HCC transition, as well as to HCC immune evasion. Therefore, uncovering the detailed mechanism governing how NASH-associated immune cells contribute to NASH progression would benefit HCC prevention and improve HCC immunotherapy efficiency. In the following review, we focused our attention on summarizing the current knowledge of the role of CD4⁺T cells in NASH and HCC progression, and discuss potential therapeutic strategies involving the targeting of CD4⁺T cells for the treatment of NASH and HCC. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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14 pages, 1016 KiB

Open AccessReview

Compilation of Evidence Supporting the Role of a T Helper 2 Reaction in the Pathogenesis of Acute Appendicitis

by Nuno Carvalho, Ana Lúcia Barreira, Susana Henriques, Margarida Ferreira, Carlos Cardoso, Carlos Luz and Paulo Matos Costa

Int. J. Mol. Sci. 2024, 25(8), 4216; https://doi.org/10.3390/ijms25084216 - 11 Apr 2024

Viewed by 1178

Abstract

Despite being the most common abdominal surgical emergency, the cause of acute appendicitis (AA) remains unclear, since in recent decades little progress has been made regarding its etiology. Obstruction of the appendicular lumen has been traditionally presented as the initial event of AA; however, this is often the exception rather than the rule, as experimental data suggest that obstruction is not an important causal factor in AA, despite possibly occurring as a consequence of the inflammatory process. Type I hypersensitivity reaction has been extensively studied, involving Th2 lymphocytes, and cytokines such as IL-4, IL-5, IL-9 and IL-13, which have well-defined functions, such as a positive-feedback effect on Th0 for differentiating into Th2 cells, recruitment of eosinophils and the release of eosinophilic proteins and the production of IgE with the activation of mast cells, with the release of proteins from their granules. Cytotoxic activity and tissue damage will be responsible for the clinical manifestation of the allergy. AA histological features are similar to those found in allergic reactions like asthma. The intestine has all the components for an allergic immune response. It has contact with hundreds of antigens daily, most of them harmless, but some can potentially induce an allergic response. In recent years, researchers have been trying to assess if allergy is a component of AA, with their latest advances in the understanding of AA as a Th2 reaction shown by the authors of this article. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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15 pages, 1366 KiB

Open AccessReview

HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation

by Qingqing Liu, Xiaoyu Yan, Yuan Yuan, Runyuan Li, Yuanxin Zhao, Jiaying Fu, Jian Wang and Jing Su

Int. J. Mol. Sci. 2024, 25(3), 1577; https://doi.org/10.3390/ijms25031577 - 27 Jan 2024

Cited by 3 | Viewed by 2398

Abstract

Systemic chronic inflammation (SCI) due to intrinsic immune over-activation is an important factor in the development of many noninfectious chronic diseases, such as neurodegenerative diseases and diabetes mellitus. Among these immune responses, macrophages are extensively involved in the regulation of inflammatory responses by virtue of their polarization plasticity; thus, dysregulation of macrophage polarization direction is one of the potential causes of the generation and maintenance of SCI. High-temperature demand protein A2 (HtrA2/Omi) is an important regulator of mitochondrial quality control, not only participating in the degradation of mis-accumulated proteins in the mitochondrial unfolded protein response (UPRmt) to maintain normal mitochondrial function through its enzymatic activity, but also participating in the regulation of mitochondrial dynamics-related protein interactions to maintain mitochondrial morphology. Recent studies have also reported the involvement of HtrA2/Omi as a novel inflammatory mediator in the regulation of the inflammatory response. HtrA2/Omi regulates the inflammatory response in BMDM by controlling TRAF2 stabilization in a collagen-induced arthritis mouse model; the lack of HtrA2 ameliorates pro-inflammatory cytokine expression in macrophages. In this review, we summarize the mechanisms by which HtrA2/Omi proteins are involved in macrophage polarization remodeling by influencing macrophage energy metabolism reprogramming through the regulation of inflammatory signaling pathways and mitochondrial quality control, elucidating the roles played by HtrA2/Omi proteins in inflammatory responses. In conclusion, interfering with HtrA2/Omi may become an important entry point for regulating macrophage polarization, providing new research space for developing HtrA2/Omi-based therapies for SCI. Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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18 pages, 961 KiB

Open AccessReview

Role of Regulatory T Cells and Their Potential Therapeutic Applications in Celiac Disease

by Alessandra Camarca, Vera Rotondi Aufiero and Giuseppe Mazzarella

Int. J. Mol. Sci. 2023, 24(19), 14434; https://doi.org/10.3390/ijms241914434 - 22 Sep 2023

Cited by 2 | Viewed by 2286

Abstract

Celiac disease (CeD) is a T-cell-mediated immune disease, in which gluten-derived peptides activate lamina propria effector CD4+ T cells. While this effector T cell subset produces proinflammatory cytokines, which cause substantial tissue injury in vivo, additional subsets of T cells exist with regulatory functions (Treg). These subsets include CD4+ type 1 regulatory T cells (Tr1) and CD4+ CD25+ T cells expressing the master transcription factor forkhead box P3 (Foxp3) that may have important implications in disease pathogenesis. In this review, we provide an overview of the current knowledge about the effects of immunomodulating cytokines on CeD inflammatory status. Moreover, we outline the main Treg cell populations found in CeD and how their regulatory activity could be influenced by the intestinal microenvironment. Finally, we discuss the Treg therapeutic potential for the development of alternative strategies to the gluten-free diet (GFD). Full article

(This article belongs to the Special Issue Role of Immune Cells in Non-infectious Inflammatory Diseases and Cancers)

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