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Immune-Mediated Diseases
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Immune-Mediated Diseases

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 12390

Special Issue Editors

Prof. Dr. Melchor Álvarez de Mon

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Guest Editor
1. Department of Medicine and Medical Specialities, IRYCYS, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain
2. Immune System Diseases-Rheumatology and Internal Medicine Service, University Hospital Príncipe de Asturias, (CIBEREHD), 28806 Alcala de Henares, Spain
Interests: immune system; systemic diseases; semiology; cytokines; translational medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Miguel Ortega

E-Mail Website
Guest Editor
Department of Medicine and Medical Specialities, IRYCYS, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain
Interests: vascular diseases; artery; venous disease; venous hypertension; heart; lymph; diabetes; immune system; translational medicine
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jorge Monserrat

E-Mail Website
Guest Editor
Department of Medicine and Medical Specialities, IRYCYS, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain
Interests: inflammation; T, B and NK cells; monocytes and dendritic cells functions applied to immune system and infection (multiorgan failure syndrome, COVID-19); autoimmunity (rheumatoid arthritis and lupus); cancer (leukemia and lung cancer); hepatology; fibromyalgia and mayor depression; expert in flow cytometry
Special Issues, Collections and Topics in MDPI journals
Dr. Miguel Ángel Alvarez de Mon

E-Mail Website
Guest Editor
Department of Medicine and Medical Specialities, IRYCYS, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain
Interests: personalized medicine; clinical medicine; new therapies; medical–patient relationship
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immune-mediated diseases constitute a broad spectrum of diseases that cause serious consequences in patients. These diseases result in a clear compromise of immune response, which can cause an abnormal functioning of organs and systems, with responses at a systemic level. In this sense, immune-mediated diseases are not known in all cellular and molecular mechanisms. In addition, the repercussions on patients themselves are severe at both social and psychoneuroendocrinological levels. In this Special Issue, we want to bring together research that will allow us to give our patients personalized and more effective medicine.

Prof. Dr. Melchor Álvarez de Mon
Dr. Miguel Ortega
Prof. Dr. Jorge Monserrat
Dr. Miguel Ángel Alvarez de Mon
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. Journal of Personalized Medicine is an international peer-reviewed open access monthly 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 2600 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-mediated inflammatory diseases (IMID)
  • integrative medicine
  • psychoneuroimmunoendocrinology (PNIE)
  • inflammation
  • T, B and NK cells
  • monocytes and dendritic cells
  • COVID-19
  • autoimmunity
  • cancer (leukemia and lung cancer)
  • flow cytometry

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Published Papers (5 papers)

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Research

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12 pages, 255 KiB  
Article
LPL rs264, PROCR rs867186 and PDGF rs974819 Gene Polymorphisms in Patients with Unstable Angina
by Damian Malinowski, Krzysztof Safranow and Andrzej Pawlik
J. Pers. Med. 2024, 14(2), 213; https://doi.org/10.3390/jpm14020213 - 16 Feb 2024
Viewed by 1481
Abstract
Background: Coronary artery disease is caused by changes in the coronary arteries due to the atherosclerotic process and thrombotic changes. A very important role in the development of the atherosclerotic process in the coronary vessels is played by the inflammatory process and the [...] Read more.
Background: Coronary artery disease is caused by changes in the coronary arteries due to the atherosclerotic process and thrombotic changes. A very important role in the development of the atherosclerotic process in the coronary vessels is played by the inflammatory process and the immune response. Due to the important role of lipids and the coagulation process in the atherosclerotic process, research has also focused on genes affecting lipid metabolism and the coagulation system. Lipoprotein lipase (LPL) is an enzyme that metabolises lipids, hydrolysing triglycerides to produce free fatty acids and glycerol. Protein C (PC) is an essential component of coagulation and fibrinolysis. It is activated on the endothelial surface by the membrane-bound thrombin-thrombomodulin complex. Platelet-derived growth factor (PDGF) has a number of important functions in processes related to fibroblast and smooth muscle cell function. Due to their influence on lipid metabolism and coagulation processes, LPL, PROCR (endothelial cell protein C receptor) and PDGF may affect the atherosclerotic process and, thus, the risk of coronary heart disease. The aim of the study was to examine the associations between the LPL rs264, PROCR rs867186 and PDGF rs974819 gene polymorphisms and the risk of unstable angina and selected clinical parameters. Methods: The study included 232 patients with unstable angina and 144 healthy subjects as the control group. Genotyping was performed using real-time PCR. Results: There were no statistically significant differences in the distribution of the polymorphisms tested between the patients with unstable angina and the control subjects. The results showed associations between the PROCR rs867186 and PDGF rs974819 polymorphisms and some clinical parameters in patients with unstable angina. In patients with the PDGF rs974819 CC genotype, there were increased values for cholesterol and LDL serum levels in comparison with patients with the PDGF rs974819 CT and TT genotypes. In patients with the PROCR rs867186 AA genotype, HDL serum levels were lower than in patients with the GA genotype. Conclusions: The results of our study did not show that the LPL rs264, PROCR rs867186 and PDGF rs974819 gene polymorphisms were significant risk factors for unstable angina in our population. The results of the study suggest that PDGF rs974819 and PROCR rs867186 may be associated with some parameters of lipid metabolism. Full article
(This article belongs to the Special Issue Immune-Mediated Diseases)
14 pages, 8675 KiB  
Article
The Immune Landscape and Molecular Subtypes of Pediatric Crohn’s Disease: Results from In Silico Analysis
by Shiyu Xiao, Wenhui Xie, Yinghui Zhang, Yan Pan and Lei Lei
J. Pers. Med. 2023, 13(4), 571; https://doi.org/10.3390/jpm13040571 - 23 Mar 2023
Cited by 3 | Viewed by 1910
Abstract
Pediatric Crohn’s disease (CD) presents a distinct phenotype from adult-onset disease. A dysregulated immune response is critical in CD pathogenesis; thus, it is clinically important to describe immune cell alterations and to identify a new molecular classification for pediatric CD. To this end, [...] Read more.
Pediatric Crohn’s disease (CD) presents a distinct phenotype from adult-onset disease. A dysregulated immune response is critical in CD pathogenesis; thus, it is clinically important to describe immune cell alterations and to identify a new molecular classification for pediatric CD. To this end, in this study, a RNA-seq derived dataset GSE101794—which contains the expression profiles of 254 treatment-naïve pediatric CD samples, including CIBERSORTx and weighted gene-co-expression network analysis (WGCNA)—were performed to estimate the ratio of immune cells and to identify modules and genes related to specific immune cell infiltration, respectively. Hub genes derived from WGCNA were further employed to create a molecular classification using unsupervised K-means clustering. In the pediatric CD samples, it was found that M2 macrophages, CD4+ memory resting T cells, CD8+ T cells, and resting mast cells were the most prominent immune cells in intestinal tissues. Then, 985 up-regulated genes and 860 down-regulated genes were identified in samples with high immune cell infiltration. Of these differential genes, 10 hub genes (APOA1, CYB5A, XPNPEP2, SLC1A7, SLC4A6, LIPE, G6PC, AGXT2, SLC13A1, and SOAT2) were associated with CD8+T cell infiltration. Clinically, the higher expression of these 10 hub genes was strongly associated with an earlier age of CD onset and colonic-type CD. Furthermore, based on these key genes, pediatric CD could be classified into three molecular subtypes, displaying a different immune landscape. Altogether, this in silico analysis provides a novel insight into the immune signature of pediatric CD, and a new classification of pediatric CD is presented, which may help us develop more personalized disease management and treatments for pediatric CD. Full article
(This article belongs to the Special Issue Immune-Mediated Diseases)
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13 pages, 6284 KiB  
Article
Resveratrol Inhibits Activation of Microglia after Stroke through Triggering Translocation of Smo to Primary Cilia
by Hongyan Liao, Jiagui Huang, Jie Liu, Yue Chen, Huimin Zhu, Xuemei Li, Jun Wen, Qin Xiang and Qin Yang
J. Pers. Med. 2023, 13(2), 268; https://doi.org/10.3390/jpm13020268 - 31 Jan 2023
Cited by 4 | Viewed by 2191
Abstract
Activated microglia act as a double-edged sword for stroke. In the acute phase of stroke, activated microglia might deteriorate neurological function. Therefore, it is of great clinical transforming potential to explore drugs or methods that can inhibit abnormal activation of microglia in the [...] Read more.
Activated microglia act as a double-edged sword for stroke. In the acute phase of stroke, activated microglia might deteriorate neurological function. Therefore, it is of great clinical transforming potential to explore drugs or methods that can inhibit abnormal activation of microglia in the acute phase of stroke to improve neurological function after stroke. Resveratrol has a potential effect of regulating microglial activation and anti-inflammation. However, the molecular mechanism of resveratrol-inhibiting microglial activation has not been fully clarified. Smoothened (Smo) belongs to the Hedgehog (Hh) signaling pathway. Smo activation is the critical step that transmits the Hh signal across the primary cilia to the cytoplasm. Moreover, activated Smo can improve neurological function via regulating oxidative stress, inflammation, apoptosis, neurogenesis, oligodendrogenesis, axonal remodeling, and so on. More studies have indicated that resveratrol can activate Smo. However, it is currently unknown whether resveratrol inhibits microglial activation via Smo. Therefore, in this study, N9 microglia in vitro and mice in vivo were used to investigate whether resveratrol inhibited microglial activation after oxygen-glucose deprivation/reoxygenation (OGD/R) or middle cerebral artery occlusion/reperfusion (MCAO/R) injury and improved functional outcome via triggering translocation of Smo in primary cilia. We definitively found that microglia had primary cilia; resveratrol partially inhibited activation and inflammation of microglia, improved functional outcome after OGD/R and MCAO/R injury, and triggered translocation of Smo to primary cilia. On the contrary, Smo antagonist cyclopamine canceled the above effects of resveratrol. The study suggested that Smo receptor might be a therapeutic target of resveratrol for contributing to inhibit microglial activation in the acute phase of stroke. Full article
(This article belongs to the Special Issue Immune-Mediated Diseases)
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Review

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21 pages, 1072 KiB  
Review
Review: A Contemporary, Multifaced Insight into Psoriasis Pathogenesis
by Rucsandra Cristina Dascălu, Andreea Lili Bărbulescu, Loredana Elena Stoica, Ștefan Cristian Dinescu, Cristina Elena Biță, Horațiu Valeriu Popoviciu, Răzvan Adrian Ionescu and Florentin Ananu Vreju
J. Pers. Med. 2024, 14(5), 535; https://doi.org/10.3390/jpm14050535 - 16 May 2024
Cited by 2 | Viewed by 2483
Abstract
Psoriasis is a chronic recurrent inflammatory autoimmune pathology with a significant genetic component and several interferences of immunological cells and their cytokines. The complex orchestration of psoriasis pathogenesis is related to the synergic effect of immune cells, polygenic alterations, autoantigens, and several other [...] Read more.
Psoriasis is a chronic recurrent inflammatory autoimmune pathology with a significant genetic component and several interferences of immunological cells and their cytokines. The complex orchestration of psoriasis pathogenesis is related to the synergic effect of immune cells, polygenic alterations, autoantigens, and several other external factors. The major act of the IL-23/IL-17 axis, strongly influencing the inflammatory pattern established during the disease activity, is visible as a continuous perpetuation of the pro-inflammatory response and keratinocyte activation and proliferation, leading to the development of psoriatic lesions. Genome-wide association studies (GWASs) offer a better view of psoriasis pathogenic pathways, with approximately one-third of psoriasis’s genetic impact on psoriasis development associated with the MHC region, with genetic loci located on chromosome 6. The most eloquent genetic factor of psoriasis, PSORS1, was identified in the MHC I site. Among the several factors involved in its complex etiology, dysbiosis, due to genetic or external stimulus, induces a burst of pro-inflammatory consequences; both the cutaneous and gut microbiome get involved in the psoriasis pathogenic process. Cutting-edge research studies and comprehensive insights into psoriasis pathogenesis, fostering novel genetic, epigenetic, and immunological factors, have generated a spectacular improvement over the past decades, securing the path toward a specific and targeted immunotherapeutic approach and delayed progression to inflammatory arthritis. This review aimed to offer insight into various domains that underline the pathogenesis of psoriasis and how they influence disease development and evolution. The pathogenesis mechanism of psoriasis is multifaceted and involves an interplay of cellular and humoral immunity, which affects susceptible microbiota and the genetic background. An in-depth understanding of the role of pathogenic factors forms the basis for developing novel and individualized therapeutic targets that can improve disease management. Full article
(This article belongs to the Special Issue Immune-Mediated Diseases)
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17 pages, 1316 KiB  
Review
Updated Views in Targeted Therapy in the Patient with Non-Small Cell Lung Cancer
by Miguel A. Ortega, Leonel Pekarek, Fátima Navarro, Oscar Fraile-Martínez, Cielo García-Montero, Miguel Ángel Álvarez-Mon, Raúl Diez-Pedrero, María del Carmen Boyano-Adánez, Luis G. Guijarro, Silvestra Barrena-Blázquez, Ana M. Gómez-Lahoz, Sergio Haro, Mónica Arroyo, Jorge Monserrat, Miguel A. Saez and Melchor Alvarez-Mon
J. Pers. Med. 2023, 13(2), 167; https://doi.org/10.3390/jpm13020167 - 17 Jan 2023
Cited by 9 | Viewed by 3561
Abstract
Non-small cell lung cancer (NSCLC) is the most frequent form of lung cancer and represents a set of histological entities that have an ominous long-term prognosis, for example, adenocarcinoma, squamous carcinoma and large cell carcinoma. Both small cell and non-small cell lung cancer [...] Read more.
Non-small cell lung cancer (NSCLC) is the most frequent form of lung cancer and represents a set of histological entities that have an ominous long-term prognosis, for example, adenocarcinoma, squamous carcinoma and large cell carcinoma. Both small cell and non-small cell lung cancer are the main causes of oncological death and the oncological diseases with the highest incidence worldwide. With regard to clinical approaches for NSCLC, several advances have been achieved in diagnosis and treatment; the analysis of different molecular markers has led to the development of new targeted therapies that have improved the prognosis for selected patients. Despite this, most patients are diagnosed in an advanced stage, presenting a limited life expectancy with an ominous short-term prognosis. Numerous molecular alterations have been described in recent years, allowing for the development of therapies directed against specific therapeutic targets. The correct identification of the expression of different molecular markers has allowed for the individualization of treatment throughout the disease course, expanding the available therapeutic arsenal. The purpose of this article is to summarize the main characteristics of NSCLC and the advances that have occurred in the use of targeted therapies, thus explaining the limitations that have been observed in the management of this disease. Full article
(This article belongs to the Special Issue Immune-Mediated Diseases)
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