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Updates in Cell and Molecular Mechanisms of Autoimmune Diseases 2.0

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: 31 August 2024 | Viewed by 6412

Special Issue Editor


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Guest Editor
Department of Medical Research, National Yang-Ming University Taiwan, Taipei, Taiwan
Interests: neonate; cytokines; T cells; epigenetics; L-arginine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is a continued issue of Special Issue “Updates in Cell and Molecular Mechanisms of Autoimmune Diseases”.

The scope of the Special Issue of “Updates in Cell and Molecular Mechanisms of Autoimmune Diseases 2.0” is to offer the possibility of collecting high-quality publications and to provide an interdisciplinary approach by submitting original papers, case series, and updated reviews on various aspects of autoimmune disorders including Kawasaki disease, type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, vaccine-mediated autoimmunity including adjuvant effect, thyroid disease, thrombosis, and post-infectious (e.g., COVID-19) autoimmunity. The cell and molecular regulations of autoimmune diseases in central and peripheral immune systems are welcome to address the aspects of cell kinetics and/or molecular dynamics, particularly balance between Th17 and Treg development, for further precision target therapy. The identifications of epigenetic and/or genetic regulation of or predisposition to autoimmune diseases are also expected to provide for prediction and prevention. Physiological pathway interactions, theranostics of extracellular vesicles, alternative therapeutic strategies, and new methods in diseases or drug treatments for autoimmune disorders are also awaited.

Prof. Dr. Kuender D. Yang
Guest Editor

Manuscript Submission Information

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Keywords

  • adjuvant effect
  • autoimmune
  • cell kinetics
  • epigenetic
  • genetic regulation
  • interdisciplinary approach
  • kawasaki disease
  • molecular mechanisms
  • post-infectious (e.g., COVID-19) autoimmunity
  • rheumatoid arthritis
  • systemic lupus erythematosus
  • theranostics of extracellular vesicles
  • thrombosis
  • thyroid disease
  • type 1 diabetes
  • vaccine-mediated autoimmunity

Published Papers (3 papers)

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Research

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16 pages, 2332 KiB  
Article
Assessing the Impact of Influenza Vaccination Timing on Experimental Arthritis: Effects on Disease Progression and Inflammatory Biomarkers
by Vera Tarjányi, Ákos Ménes, Leila Hamid, Andrea Kurucz, Dániel Priksz, Balázs Varga, Rudolf Gesztelyi, Rita Kiss, Ádám István Horváth, Nikolett Szentes, Zsuzsanna Helyes, Zoltán Szilvássy and Mariann Bombicz
Int. J. Mol. Sci. 2024, 25(6), 3292; https://doi.org/10.3390/ijms25063292 - 14 Mar 2024
Viewed by 677
Abstract
Numerous studies have indicated a link between vaccines and the exacerbation of autoimmune diseases including rheumatoid arthritis (RA). However, there is no consensus in clinical practice regarding the optimal timing of immunization. Therefore, this study aimed to investigate the impact of the 3Fluart [...] Read more.
Numerous studies have indicated a link between vaccines and the exacerbation of autoimmune diseases including rheumatoid arthritis (RA). However, there is no consensus in clinical practice regarding the optimal timing of immunization. Therefore, this study aimed to investigate the impact of the 3Fluart influenza vaccine on the complete Freund’s adjuvant (CFA)-induced chronic arthritis rat model and to identify new biomarkers with clinical utility. CFA was injected into the plantar surface of one hind paw and the root of the tail on day 0, and the tail root injection was repeated on day 1. Flu vaccination was performed on day 1 or 7. Paw volume was measured by plethysmometry, mechanonociceptive threshold by dynamic plantar aesthesiometry, neutrophil myeloperoxidase (MPO) activity, and vascular leakage using in vivo optical imaging throughout the 21-day experiment. Inflammatory markers were determined by Western blot and histopathology. CFA-induced swelling, an increase in MPO activity, plasma extravasation in the tibiotarsal joint. Mechanical hyperalgesia of the hind paw was observed 3 days after the injection, which gradually decreased. Co-administration of the flu vaccine on day 7 but not on day 1 resulted in significantly increased heme oxygenase 1 (HO-1) expression. The influenza vaccination appears to have a limited impact on the progression and severity of the inflammatory response and associated pain. Nevertheless, delayed vaccination could alter the disease activity, as indicated by the findings from assessments of edema and inflammatory biomarkers. HO-1 may serve as a potential marker for the severity of inflammation, particularly in the case of delayed vaccination. However, further investigation is needed to fully understand the regulation and role of HO-1, a task that falls outside the scope of the current study. Full article
(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases 2.0)
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15 pages, 2481 KiB  
Article
Preliminary Evidence of the Differential Expression of Human Endogenous Retroviruses in Kawasaki Disease and SARS-CoV-2-Associated Multisystem Inflammatory Syndrome in Children
by Emanuela Balestrieri, Elena Corinaldesi, Marianna Fabi, Chiara Cipriani, Martina Giudice, Allegra Conti, Antonella Minutolo, Vita Petrone, Marialaura Fanelli, Martino Tony Miele, Laura Andreozzi, Fiorentina Guida, Emanuele Filice, Matteo Meli, Sandro Grelli, Guido Rasi, Nicola Toschi, Francesco Torcetta, Claudia Matteucci, Marcello Lanari and Paola Sinibaldi-Vallebonaadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(20), 15086; https://doi.org/10.3390/ijms242015086 - 11 Oct 2023
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Abstract
Multisystem inflammatory syndrome in children (MIS-C) is a postinfectious sequela of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some clinical features overlapping with Kawasaki disease (KD). Our research group and others have highlighted that the spike protein of SARS-CoV-2 can trigger the [...] Read more.
Multisystem inflammatory syndrome in children (MIS-C) is a postinfectious sequela of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some clinical features overlapping with Kawasaki disease (KD). Our research group and others have highlighted that the spike protein of SARS-CoV-2 can trigger the activation of human endogenous retroviruses (HERVs), which in turn induces inflammatory and immune reactions, suggesting HERVs as contributing factors in COVID-19 immunopathology. With the aim to identify new factors involved in the processes underlying KD and MIS-C, we analysed the transcriptional levels of HERVs, HERV-related genes, and immune mediators in children during the acute and subacute phases compared with COVID-19 paediatric patients and healthy controls. The results showed higher levels of HERV-W, HERV-K, Syn-1, and ASCT-1/2 in KD, MIS-C, and COV patients, while higher levels of Syn-2 and MFSD2A were found only in MIS-C patients. Moreover, KD and MIS-C shared the dysregulation of several inflammatory and regulatory cytokines. Interestingly, in MIS-C patients, negative correlations have been found between HERV-W and IL-10 and between Syn-2 and IL-10, while positive correlations have been found between HERV-K and IL-10. In addition, HERV-W expression positively correlated with the C-reactive protein. This pilot study supports the role of HERVs in inflammatory diseases, suggesting their interplay with the immune system in this setting. The elevated expression of Syn-2 and MFSD2A seems to be a distinctive trait of MIS-C patients, allowing to distinguish them from KD ones. The understanding of pathological mechanisms can lead to the best available treatment for these two diseases, limiting complications and serious outcomes. Full article
(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases 2.0)
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Review

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16 pages, 1112 KiB  
Review
Diagnosis, Progress, and Treatment Update of Kawasaki Disease
by Ho-Chang Kuo
Int. J. Mol. Sci. 2023, 24(18), 13948; https://doi.org/10.3390/ijms241813948 - 11 Sep 2023
Cited by 4 | Viewed by 2981
Abstract
Kawasaki disease (KD) is an acute inflammatory disorder that primarily affects children and can lead to coronary artery lesions (CAL) if not diagnosed and treated promptly. The original clinical criteria for diagnosing KD were reported by Dr. Tomisaku Kawasaki in 1967 and have [...] Read more.
Kawasaki disease (KD) is an acute inflammatory disorder that primarily affects children and can lead to coronary artery lesions (CAL) if not diagnosed and treated promptly. The original clinical criteria for diagnosing KD were reported by Dr. Tomisaku Kawasaki in 1967 and have been used for decades. However, research since then has highlighted the limitations of relying solely on these criteria, as they might lead to underdiagnosis or delayed diagnosis, potentially increasing the risk of coronary artery complications. This review appears to discuss several important aspects related to KD diagnosis and management. The current diagnostic methods for KD might need updates, especially considering cases that do not fit the typical clinical criteria. Recognizing diagnostic pitfalls and distinguishing KD from other conditions that might have similar clinical presentations is essential. The differences and similarities between KD and Multisystem Inflammatory Syndrome in Children (MIS-C), another inflammatory condition that has been associated with COVID-19, were also reviewed. The review explores the potential role of eosinophil count, new biomarkers, microRNA panels, and scoring systems in aiding the diagnosis of KD. Overall, the review article provides a comprehensive overview of the evolving landscape of KD diagnosis and management, incorporating new diagnostic methods, biomarkers, and treatment approaches to improve patient outcomes and reduce the risk of complications. Full article
(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases 2.0)
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