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Cells
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Immune Biomarkers of Chronic Lung Diseases and Lung Cancer
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Immune Biomarkers of Chronic Lung Diseases and Lung Cancer

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

Deadline for manuscript submissions: closed (27 January 2023) | Viewed by 9920

Special Issue Editors

Dr. Iwona Kwiecień

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Guest Editor
Department of Internal Medicine and Hematology, Laboratory of Flow Cytometry, Military Institute of Medicine, Warsaw, Poland
Interests: lung cancer; flow cytometry; cancer cells; immunohistochemistry; cancer immunology; cancer biomarkers; clinical immunology; lymphocytes; macrophage; immunology
Dr. Agata Raniszewska

E-Mail Website
Guest Editor
Department of Internal Medicine and Hematology, Laboratory of Flow Cytometry, Military Institute of Medicine, Warsaw, Poland
Interests: immunophenotyping; flow cytometry; PCR; gene sequencing; cellular immunology; cancer immunology
Prof. Dr. Joanna Domagala-Kulawik

E-Mail Website
Guest Editor
Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Warsaw, Poland
Interests: lung cancer; COPD; lung immunology; interstitial lung diseases; brochoalveolar lavage

Special Issue Information

Dear Colleagues,

The development of personalized medicine naturally forces a change in the diagnostic approach to lung cancer and chronic lung diseases, which is possible thanks to the discovery and study of biomarkers. Immunological biomarkers can create a characteristic picture of cellular features that can be used in therapy, but also for disease identification and evaluation of micrometastases or residual disease. With the recognition of new biomarkers, in cancer therapeutics, the past 5 years have seen something of a revolution in immunologically targeted approaches to treatment, including the development of a novel therapeutic drug class of immune checkpoint-blocking antibodies.  

With this in mind, many common respiratory diseases, including pneumonia, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and lung cancer require a new diagnostic perspective. There is evidence that COPD and pulmonary fibrosis are possibly complicated by lung cancer development and importantly change the course of pulmonary malignancies. Thus, the immune background of these conditions requires special attention.  

With the number of publications on immune biomarkers rapidly increasing, now is the time to take a broad perspective of the field, putting emphasis not only on the use of biomarkers to create new therapies, but also on improving diagnostics using immunological biomarkers.

Prof. Dr. Joanna Domagala-Kulawik
Dr. Agata Raniszewska
Dr. Iwona Kwiecień
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. 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

  • lung cancer
  • cell biomarkers
  • flow cytometry
  • antigen-specific assays
  • non-antigen-specific assays, Immune
  • chronic lung diseases COPD
  • interstitial lung diseases
  • asthma
  • rare lung diseases

Published Papers (4 papers)

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Research

18 pages, 2366 KiB  
Article
Comparative Analysis of FCGR Gene Polymorphism in Pulmonary Sarcoidosis and Tuberculosis
by Marlena Typiak, Bartłomiej Rękawiecki, Krzysztof Rębała and Anna Dubaniewicz
Cells 2023, 12(9), 1221; https://doi.org/10.3390/cells12091221 - 23 Apr 2023
Cited by 2 | Viewed by 1135
Abstract
The clinical outcome of sarcoidosis (SA) is very similar to tuberculosis (TB); however, they are treated differently and should not be confused. In search for their biomarkers, we have previously revealed changes in the phagocytic activity of monocytes in sarcoidosis and tuberculosis. On [...] Read more.
The clinical outcome of sarcoidosis (SA) is very similar to tuberculosis (TB); however, they are treated differently and should not be confused. In search for their biomarkers, we have previously revealed changes in the phagocytic activity of monocytes in sarcoidosis and tuberculosis. On these monocytes we found a higher expression of receptors for the Fc fragment of immunoglobulin G (FcγR) in SA and TB patients vs. healthy controls. FcγRs are responsible for the binding of immune complexes (ICs) to initiate an (auto)immune response and for ICs clearance. Surprisingly, our SA patients had a high blood level of ICs, despite the abundant presence of FcγRs. It pointed to FcγR disfunction, presumably caused by the polymorphism of their (FCGR) genes. Therefore, we present here an analysis of the occurrence of FCGR2A, FCGR2B, FCGR2C, FCGR3A and FCGR3B variants in Caucasian SA and TB patients, and healthy individuals with the use of polymerase chain reaction (PCR) and real-time PCR. The presented data point to a possibility of supporting the differential diagnosis of SA and TB by analyzing FCGR2C, FCGR3A and FCGR3B polymorphism, while for severe stages of SA also by studying FCGR2A variants. Additionally, the genotyping of FCGR2A and FCGR3B might serve as a marker of SA progression. Full article
(This article belongs to the Special Issue Immune Biomarkers of Chronic Lung Diseases and Lung Cancer)
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8 pages, 554 KiB  
Communication
Targeting YAP/TAZ in Combination with PD-L1 Immune Checkpoint Inhibitors in Non-Small Cell Lung Cancer (NSCLC)
by Kostas A. Papavassiliou, Georgios Marinos and Athanasios G. Papavassiliou
Cells 2023, 12(6), 871; https://doi.org/10.3390/cells12060871 - 10 Mar 2023
Cited by 6 | Viewed by 4197
Abstract
The survival of non-small cell lung cancer (NSCLC) patients has improved in the last decade as a result of introducing new therapeutics, such as immune checkpoint inhibitors, in the clinic. Still, some NSCLC patients do not benefit from these therapies due to intrinsic [...] Read more.
The survival of non-small cell lung cancer (NSCLC) patients has improved in the last decade as a result of introducing new therapeutics, such as immune checkpoint inhibitors, in the clinic. Still, some NSCLC patients do not benefit from these therapies due to intrinsic resistance or the development of acquired resistance and their malignant disease progresses. Further research on the molecular underpinnings of NSCLC pathobiology is required in order to discover clinically relevant molecular targets that regulate tumor immunity and to develop reasonable therapeutic combinations that will promote the efficacy of immune checkpoint inhibitors. Yes-associated Protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), the final effectors of the Hippo signaling transduction pathway, are emerging as key players in NSCLC development and progression. Herein, we overview studies that have investigated the oncogenic role of YAP/TAZ in NSCLC, focusing on immune evasion, and highlight the therapeutic potential of combining YAP/TAZ inhibitory agents with immune checkpoint inhibitors for the management of NSCLC patients. Full article
(This article belongs to the Special Issue Immune Biomarkers of Chronic Lung Diseases and Lung Cancer)
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16 pages, 4212 KiB  
Article
Prognostic Role of Soluble and Extracellular Vesicle-Associated PD-L1, B7-H3 and B7-H4 in Non-Small Cell Lung Cancer Patients Treated with Immune Checkpoint Inhibitors
by Carlo Genova, Roberta Tasso, Alessandra Rosa, Giovanni Rossi, Daniele Reverberi, Vincenzo Fontana, Silvia Marconi, Michela Croce, Maria Giovanna Dal Bello, Chiara Dellepiane, Marco Tagliamento, Maria Chiara Ciferri, Lodovica Zullo, Alessandro Fedeli, Angela Alama, Katia Cortese, Chiara Gentili, Eugenia Cella, Giorgia Anselmi, Marco Mora, Giulia Barletta, Erika Rijavec, Francesco Grossi, Paolo Pronzato and Simona Cocoadd Show full author list remove Hide full author list
Cells 2023, 12(6), 832; https://doi.org/10.3390/cells12060832 - 8 Mar 2023
Cited by 11 | Viewed by 2539
Abstract
The treatment of non-small cell lung cancer (NSCLC) has changed dramatically with the advent of immune checkpoint inhibitors (ICIs). Despite encouraging results, their efficacy remains limited to a subgroup of patients. Circulating immune checkpoints in soluble (s) form and associated with extracellular vesicles [...] Read more.
The treatment of non-small cell lung cancer (NSCLC) has changed dramatically with the advent of immune checkpoint inhibitors (ICIs). Despite encouraging results, their efficacy remains limited to a subgroup of patients. Circulating immune checkpoints in soluble (s) form and associated with extracellular vesicles (EVs) represent promising markers, especially in ICI-based therapeutic settings. We evaluated the prognostic role of PD-L1 and of two B7 family members (B7-H3, B7-H4), both soluble and EV-associated, in a cohort of advanced NSCLC patients treated with first- (n = 56) or second-line (n = 126) ICIs. In treatment-naïve patients, high baseline concentrations of sPD-L1 (>24.2 pg/mL) were linked to worse survival, whereas high levels of sB7-H3 (>0.5 ng/mL) and sB7-H4 (>63.9 pg/mL) were associated with better outcomes. EV characterization confirmed the presence of EVs positive for PD-L1 and B7-H3, while only a small portion of EVs expressed B7-H4. The comparison between biomarker levels at the baseline and in the first radiological assessment under ICI-based treatment showed a significant decrease in EV-PD-L1 and an increase in EV-B7H3 in patients in the disease response to ICIs. Our study shows that sPD-L1, sB7-H3 and sB7-H4 levels are emerging prognostic markers in patients with advanced NSCLC treated with ICIs and suggests potential EV involvement in the disease response to ICIs. Full article
(This article belongs to the Special Issue Immune Biomarkers of Chronic Lung Diseases and Lung Cancer)
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16 pages, 7638 KiB  
Article
Study of the Regulatory Mechanism of miR-26a-5p in Allergic Asthma
by Jinnan Zhong, Min Liu, Shi Chen, Shuang Liu, Fajiu Li and Chenghong Li
Cells 2023, 12(1), 38; https://doi.org/10.3390/cells12010038 - 22 Dec 2022
Cited by 4 | Viewed by 1475
Abstract
Objective: Allergic asthma is a growing burden on national public health services due to its high prevalence. The aim of this experiment was to investigate whether miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice through the regulation of target genes. [...] Read more.
Objective: Allergic asthma is a growing burden on national public health services due to its high prevalence. The aim of this experiment was to investigate whether miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice through the regulation of target genes. Methods: Screening for differentially expressed miRNAs in asthma model mice was carried out by constructing a mouse model of allergic asthma. qRT-PCR was performed to determine candidate miRNAs in each group of bronchial tissues. Western blot detection of the expression levels of predicted candidate target genes in each group of bronchial tissues was conducted. A dual luciferase assay was performed to validate the binding of miR-26a-5p to target genes. Fibronectin, a marker of cellular fibrosis, was detected via flow cytometry. CCK8 and BrdU staining were used to detect the proliferation ability of each group of cells. Results: miR-26a-5p is able to target and bind to ABL2 3′-UTR, MMP16 3′-UTR and PDE7A 3′-UTR sequences. After interference with miR-26a-5p, improved bronchial histopathology and reduced peribronchial collagen deposition were found. Compared with the model group, interference with miR-26a-5p reduced lung fibrosis, decreased fibroblasts and increased apoptosis in mouse bronchial tissues; overexpression of miR-26a-5p decreased apoptosis in mouse bronchial tissues. Compared with the model group, the serum levels of IL-4, IL-5, IL-13 and I IFN-γ were decreased in the miR-26a-5p inhibitor group and increased in the miR-26a-5p mimic group. The immunohistochemical results showed that the expression of ABL2, MMP16 and PDE7A was significantly reduced after intervention with miR-26a-5p. Compared with the model group, the apoptosis rate of cells in the miR-26a-5p inhibitor group of the allergic asthma model was upregulated, the levels of IL-4, IL-5, IL-13, IFN-γ and ROS were decreased, the expression of the miRNA and proteins of ABL2, MMP16 and PDE7A was decreased, the expression of LC3A and P62 was significantly increased and the expression of LC3B, Beclin1, Atg5 and fibrosis markers collagen I and α-SMA was decreased. Conclusion: miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice by regulating target genes. Full article
(This article belongs to the Special Issue Immune Biomarkers of Chronic Lung Diseases and Lung Cancer)
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