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Biomedicines
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10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases
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10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 10477

Special Issue Editor

Prof. Dr. Giuseppe Murdaca

E-Mail Website
Guest Editor
Head of Allergology and Clinical Immunology Unit, Department of Internal Medicine, University of Genoa and San Bartolomeo Hospital, Sarzana, Italy
Interests: immunodeficiency; autoimmunity; neuro-endocrino-immunology; pharmacogenomics; soluble molecules; immune-mediated diseases; allergies; vaccines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases are multifactorial conditions, in which both genetic and environmental factors play a crucial role. Although they are characterized by different phenotypes, these disorders often share a common and complex environment of cytokines involved in their pathogenesis. Among them, interleukin (IL)-31 and IL-33 have been extensively studied, leading to the most recent theory of an "IL-31 / IL-33 axis" that could be involved in the genesis of autoimmune diseases. In addition to the latter, also other molecules belonging to the class of "alarmins", including defensins (α, β), cathelicidin / LL-37, the high mobility group box-1 (HMGB1) and heat shock proteins (HSP) IL-1α and S100 are involved in the genesis of the pathogenetic mechanisms underlying various autoimmune diseases, as well as in the progression and chemoresistance of some forms of tumors. More recent studies have focused on the role of the gut microbiome in shaping the immune system, contributing to the pathogenesis of many diseases involving the whole organism. Similarly, 1.25 (OH) 2D3 also plays a key role in modulating the immune response, on which it acts through binding to the vitamin D receptor (VDR). In some autoimmune diseases such as systemic sclerosis (SSc) and systemic lupus erythematosus (SLE) the role of the human leukocyte G antigen (HLA-G) has been recognized in the complex immunological pathogenesis of these two autoimmune diseases, where it is expressed in different cell populations such as T lymphocytes, NK cells and APCs. Finally, a growing interest concerns miRNAs, which alterations and polymorphisms have been found to be involved in the pathogenesis of autoimmune diseases, paving the way for the identification of new therapeutic approaches in the future.

Dr. Giuseppe Murdaca
Guest Editor

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. Biomedicines 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

  • IL-31 / IL-33 axis and autoimmune diseases
  • alarmins and autoimmune diseases
  • microbiome and autoimmune diseases
  • vitamin D and autoimmune diseases
  • HLA-G and autoimmune diseases
  • miRNA and autoimmune diseases

Related Special Issue

Published Papers (4 papers)

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Research

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17 pages, 7588 KiB  
Article
Inactivation of Yes-Associated Protein Mediates Trophoblast Dysfunction: A New Mechanism of Pregnancy Loss Associated with Anti-Phospholipid Antibodies?
by Zengshu Huang, Zhijing Tang, Haiyun Guan, Wingting Leung, Lu Wang, Hexia Xia and Wei Zhang
Biomedicines 2022, 10(12), 3296; https://doi.org/10.3390/biomedicines10123296 - 19 Dec 2022
Cited by 2 | Viewed by 1584
Abstract
Pregnancy morbidity induced by anti-phospholipid antibodies (aPL+/PM+) is mainly thought to arise from placental abnormalities. We attempted to investigate the effect of aPL on the activity of Yes-associated protein (YAP) in the trophoblast and how YAP regulated human trophoblasts function. Thus, HTR-8 cells [...] Read more.
Pregnancy morbidity induced by anti-phospholipid antibodies (aPL+/PM+) is mainly thought to arise from placental abnormalities. We attempted to investigate the effect of aPL on the activity of Yes-associated protein (YAP) in the trophoblast and how YAP regulated human trophoblasts function. Thus, HTR-8 cells were treated with IgG purified from aPL+/PM+ women or normal controls. We found that aPL+/PM+ IgG impacted YAP activity via abrogating YAP expression. Further investigation of the anti-β2GPI-IgG/β2GPI complex showed an inhibition of nuclear YAP level and translocation in a dose-dependent manner, which might be rescued by progesterone in HTR-8 cells. YAP overexpression or knockdown HTR-8 cells were established for the evaluation of cell function and related gene expression in vitro. Loss of YAP arrested cell cycles in the G2/M phase, accelerated cell apoptosis by increasing the ratio of Bax/Bcl2, and disrupted MMP2/9-mediated cell migration and angiogenesis tube formation by VEGF. These findings support a new mechanism of PM associated with aPL through which YAP inactivation induced by aPL perturbs the trophoblast cell cycle, apoptosis, migration, and angiogenesis, finally developing into pregnancy failure. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases)
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20 pages, 2638 KiB  
Article
Hydroxychloroquine on the Pulmonary Vascular Diseases in Interstitial Lung Disease: Immunologic Effects, and Virus Interplay
by Jun-Jun Yeh, Shih-Hueh Syue, Yi-Fun Sun, Yi-Ting Yeh, Ya-Chi Zheng, Cheng-Li Lin, Chung Y. Hsu and Chia-Hung Kao
Biomedicines 2022, 10(6), 1290; https://doi.org/10.3390/biomedicines10061290 - 31 May 2022
Viewed by 2254
Abstract
To investigate the effects of hydroxychloroquine (HCQ) drug use on the risk of pulmonary vascular disease (PVD) in an interstitial lung disease cohort (ILD cohort, ILD+ virus infection), we retrospectively enrolled the ILD cohort with HCQ (HCQ users, N = 4703) and the [...] Read more.
To investigate the effects of hydroxychloroquine (HCQ) drug use on the risk of pulmonary vascular disease (PVD) in an interstitial lung disease cohort (ILD cohort, ILD+ virus infection), we retrospectively enrolled the ILD cohort with HCQ (HCQ users, N = 4703) and the ILD cohort without HCQ (non-HCQ users, N = 4703) by time-dependence after propensity score matching. Cox models were used to analyze the risk of PVD. We calculated the adjusted hazard ratios (aHRs) and their 95% confidence intervals (CIs) for PVD after adjusting for sex, age, comorbidities, index date and immunosuppressants, such as steroids, etc. Compared with the HCQ nonusers, in HCQ users, the aHRs (95% CIs) for PVD were (2.24 (1.42, 3.54)), and the women’s aHRs for PVD were (2.54, (1.49, 4.35)). The aHRs based on the days of HCQ use for PVD of 28–30 days, 31–120 days, and >120 days were (1.27 (0.81, 1.99)), (3.00 (1.81, 4.87)) and (3.83 (2.46, 5.97)), respectively. The medium or long-term use of HCQ or young women receiving HCQ were associated with a higher aHR for PVD in the ILD cohort. These findings indicated interplay of the primary immunologic effect of ILD, comorbidities, women, age and virus in the HCQ users. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases)
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Review

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24 pages, 866 KiB  
Review
Genes and Microbiota Interaction in Monogenic Autoimmune Disorders
by Federica Costa, Eleonora Beltrami, Simona Mellone, Sara Sacchetti, Elena Boggio, Casimiro Luca Gigliotti, Ian Stoppa, Umberto Dianzani, Roberta Rolla and Mara Giordano
Biomedicines 2023, 11(4), 1127; https://doi.org/10.3390/biomedicines11041127 - 08 Apr 2023
Cited by 2 | Viewed by 1500
Abstract
Monogenic autoimmune disorders represent an important tool to understand the mechanisms behind central and peripheral immune tolerance. Multiple factors, both genetic and environmental, are known to be involved in the alteration of the immune activation/immune tolerance homeostasis typical of these disorders, making it [...] Read more.
Monogenic autoimmune disorders represent an important tool to understand the mechanisms behind central and peripheral immune tolerance. Multiple factors, both genetic and environmental, are known to be involved in the alteration of the immune activation/immune tolerance homeostasis typical of these disorders, making it difficult to control the disease. The latest advances in genetic analysis have contributed to a better and more rapid diagnosis, although the management remains confined to the treatment of clinical manifestations, as there are limited studies on rare diseases. Recently, the correlation between microbiota composition and the onset of autoimmune disorders has been investigated, thus opening up new perspectives on the cure of monogenic autoimmune diseases. In this review, we will summarize the main genetic features of both organ-specific and systemic monogenic autoimmune diseases, reporting on the available literature data on microbiota alterations in these patients. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases)
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12 pages, 852 KiB  
Review
Prevalence of Autoimmune and Autoinflammatory Diseases in Chronic Urticaria: Pathogenetic, Diagnostic and Therapeutic Implications
by Giuseppe Murdaca, Francesca Paladin, Matteo Borro, Luisa Ricciardi and Sebastiano Gangemi
Biomedicines 2023, 11(2), 410; https://doi.org/10.3390/biomedicines11020410 - 30 Jan 2023
Viewed by 4331
Abstract
Chronic spontaneous urticaria (CSU) is defined as the almost daily occurrence of widespread wheals, angioedema, or both, for more than 6 weeks. It affects 1–2% of the general population, with a higher prevalence in female patients, and is more frequent patients over 20 [...] Read more.
Chronic spontaneous urticaria (CSU) is defined as the almost daily occurrence of widespread wheals, angioedema, or both, for more than 6 weeks. It affects 1–2% of the general population, with a higher prevalence in female patients, and is more frequent patients over 20 years of age. More than half of all cases of chronic idiopathic urticaria are thought to occur due to an autoimmune mechanism, specifically the production of autoantibodies against the high-affinity immunoglobulin E (IgE) receptor (FcεRI). The quality of life in these patients is often greatly compromised, also due to the onset of comorbidities represented by other autoimmune diseases, such as thyroid disease, rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, celiac disease, and type 1 diabetes, among others. This review aimed to analyze the close correlation between CSU and some autoimmune and autoinflammatory diseases, in order to encourage a multidisciplinary and multimorbid approach to the patient affected by CSU, which allows not only control of the natural course of the disease, but also any associated comorbidities. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines-Immunopathogenesis of Autoimmune Diseases)
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