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Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition
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Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition

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 September 2025 | Viewed by 7532

Special Issue Editors

Prof. Dr. Yves Renaudineau

E-Mail Website
Guest Editor
Laboratory of Immunology, CHU Purpan Toulouse, INSERM U1291, CNRS U5051, University Toulouse III, Toulouse, France
Interests: autoimmune diseases; immunology; infection; immunotherapy
Special Issues, Collections and Topics in MDPI journals
Dr. Dirk Roggenbuck

E-Mail Website
Guest Editor
Institute of Biotechnology, Faculty Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, 01968 Senftenberg, Germany
Interests: molecular diagnostics; quality management; autoimmune diseases; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, dedicated to autoimmunity, attempts to present a comprehensive overview of autoimmune diseases (ADs) and how the immune system self-targets in different conditions according to a balance determined by the genetic predisposition of the host, its gender, epigenetic factors, environmental circumstances, and other co-factors. Moreover, current knowledge from human and animal models is welcome regarding the pathogenic mechanisms of autoimmune diseases, clinical aspects of specific autoimmune diseases, as well as insights regarding biomarkers and specific therapies.

Prof. Dr. Yves Renaudineau
Dr. Dirk Roggenbuck
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • autoimmunity
  • autoimmune diseases
  • immunotherapy
  • biomarkers
  • pathogenic mechanisms

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Related Special Issue

Published Papers (5 papers)

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Research

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12 pages, 697 KB  
Article
Dietary Gluten-Free Regimen Does Not Affect the Suppression of the Inflammatory Response in the Arachidonic Acid Cascade in Hashimoto’s Disease
by Małgorzata Szczuko, Lidia Kwiatkowska, Urszula Szczuko, Leon Rudak, Karina Ryterska, Anhelli Syrenicz, Jakub Pobłocki and Arleta Drozd
Int. J. Mol. Sci. 2025, 26(13), 6507; https://doi.org/10.3390/ijms26136507 - 6 Jul 2025
Viewed by 768
Abstract
The incidence of Hashimoto’s disease (HD) increases with age and in people who have other autoimmune diseases. It is characterized by lymphocytic infiltration, fibrosis, and atrophy of the thyroid parenchyma with the simultaneous presence of thyroid peroxidase antibodies (ATPO) and/or thyroglobulin antibodies (ATG). [...] Read more.
The incidence of Hashimoto’s disease (HD) increases with age and in people who have other autoimmune diseases. It is characterized by lymphocytic infiltration, fibrosis, and atrophy of the thyroid parenchyma with the simultaneous presence of thyroid peroxidase antibodies (ATPO) and/or thyroglobulin antibodies (ATG). Eicosanoids are formed via the cyclooxygenase (COX), lipoxygenase (LOX), and monooxygenase (CYP450) pathways with arachidonic acid (ARA), resulting in the production of epoxyeicosatrienoic acids (EETs) or hydroxyeicosatetraenoic acids (HETEs). These eicosanoids can act in an autocrine or paracrine manner on target cells. This study aimed to examine whether a gluten-free diet (GFD) can modulate the enzymatic pathways of the pro-inflammatory ARA cascade. The study material consisted of serum samples from Caucasian female patients with HD aged 18–55 years. Participants were enrolled in the study based on the presence of an ultrasound characteristic of HD, and elevated serum levels of anti-thyroid peroxidase antibodies and anti-thyroglobulin antibodies. Patients with confirmed celiac disease did not participate in the study. A total of 78 samples were analyzed, with 39 collected after 3 months of following a GFD. Eicosanoids (thromboxane B2, prostaglandin E2, leukotriene B4, and 16R-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid (16-RS HETE)) were extracted using high-performance liquid chromatography. The contribution of leukotriene (LTB) was analyzed in the LOX pathway, prostaglandins (PGE2) and thromboxane (TXB2) were selected for the involvement of the COX pathway, and 16RS HETE was used for the CYP450 pathway. All parameters were analyzed before and after a 3-month dietary intervention that included a gluten-free diet. In the obtained results, only one mediator, leukotriene B4, was significant (p < 0.05). The mean level on the initial visit was 0.202 ± 0.11 (SD), while it was 0.421 ± 0.27 (SD) on the subsequent visit, indicating a significant increase in its level after implementing a GFD. Although there was a trend in the CYP 450 pathway of decreased 16-RS HETE, the presented correlations show that thromboxane B4 and 16RS-HETE were positively correlated with the body mass and body fat mass of the examined patients. There was a trend in the CYP 450 pathway of decreased 16-RS HETE after GFD. Thromboxane B4 and 16RS-HETE levels before GFD were positively correlated with the body mass and body fat mass of the examined patients. A gluten-free diet in HD does not suppress the synthetic pathways of LOX, COX, or cytochrome P450 (CYP450). The level of adipose tissue has a greater impact on the inflammatory processes in HD than a gluten-free diet. This study does not confirm the suppressive effect of a gluten-free diet on the pro-inflammatory arachidonic acid cascade in any of the three analyzed mediator synthesis LOX, COX, CYP450 pathways. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition)
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23 pages, 1695 KB  
Article
Prediction of Extraintestinal Manifestations in Inflammatory Bowel Disease Using Clinical and Genetic Variables with Machine Learning in a Latin IBD Group
by Tamara Pérez-Jeldres, Paula Reyes-Pérez, Patricio Gonzalez-Hormazabal, Cristóbal Avendano, Roberto Segovia Melero, Lorena Azocar, Veronica Silva, Andres De La Vega, Elizabeth Arriagada, Elisa Hernandez, Nataly Aguilar, Carolina Pavez-Ovalle, Cristian Hernández-Rocha, Roberto Candia, Juan Francisco Miquel, Manuel Alvarez-Lobos, Ivania Valdes, Alejandra Medina-Rivera and Maria Leonor Bustamante
Int. J. Mol. Sci. 2025, 26(12), 5741; https://doi.org/10.3390/ijms26125741 - 15 Jun 2025
Viewed by 762
Abstract
Extraintestinal manifestations (EIMs) significantly increase morbidity in inflammatory bowel disease (IBD) patients. In this study, we examined clinical and genetic factors associated with EIMs in 414 Latin IBD patients, utilizing machine learning for predictive modeling. In our IBD group (314 ulcerative colitis (UC) [...] Read more.
Extraintestinal manifestations (EIMs) significantly increase morbidity in inflammatory bowel disease (IBD) patients. In this study, we examined clinical and genetic factors associated with EIMs in 414 Latin IBD patients, utilizing machine learning for predictive modeling. In our IBD group (314 ulcerative colitis (UC) and 100 Crohn’s disease (CD) patients), EIM presence was assessed. Clinical differences between patients with and without EIMs were analyzed using Chi-square and Mann–Whitney U tests. Based on the genetic data of 232 patients, we identified variants linked to EIMs, and the polygenic risk score (PRS) was calculated. A machine learning approach based on logistic regression (LR), random forest (RF), and gradient boosting (GB) models was employed for predicting EIMs. EIMs were present in 29% (120/414) of patients. EIM patients were older (52 vs. 45 years, p = 0.01) and were more likely to have a family history of IBD (p = 0.02) or use anti-TNF therapy (p = 0.01). EIMs were more common in patients with CD than in those with UC without reaching statistical significance (p = 0.06). Four genetic variants were associated with EIM risk (rs9936833, rs4410871, rs3132680, and rs3823417). While the PRS showed limited predictive power (AUC = 0.69), the LR, GB, and RF models demonstrated good predictive capabilities. Approximately one-third of IBD patients experienced EIMs. Significant risk factors included genetic variants, family history, age, and anti-TNF therapy, with predictive models effectively identifying EIM risk. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition)
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12 pages, 1582 KB  
Article
Increased Cytokine Levels in Seronegative Myositis: Potential Th17 Immune Response Implications
by Andrea Aguilar-Vazquez, Efrain Chavarria-Avila, José Manuel Gutiérrez-Hernández, Guillermo Toriz-González, Mario Salazar-Paramo, Gabriel Medrano-Ramirez, Steven Vargas-Cañas, Oscar Pizano-Martinez, Cynthia-Alejandra Gomez-Rios, Christian Juarez-Gomez, José-David Medina-Preciado, Maribell Cabrera-López, Edgar-Federico Quirarte-Tovar, Ligia Magaña-García, Alejandra-Rubí García-Gallardo, Edy-David Rubio-Arellano and Monica Vazquez-Del Mercado
Int. J. Mol. Sci. 2024, 25(20), 11061; https://doi.org/10.3390/ijms252011061 - 15 Oct 2024
Viewed by 1726
Abstract
Th17 cells are known for producing IL-17 and their role in the pathogenesis of various autoimmune diseases, including myositis. Likewise, the participation of the IL-23/IL-17 pathway in autoimmunity has been confirmed. In this study, we aimed to evaluate the behavior of cytokines in [...] Read more.
Th17 cells are known for producing IL-17 and their role in the pathogenesis of various autoimmune diseases, including myositis. Likewise, the participation of the IL-23/IL-17 pathway in autoimmunity has been confirmed. In this study, we aimed to evaluate the behavior of cytokines in myositis, focusing on the autoantibodies profile and the myositis core set measures. Twenty-five myositis patients were enrolled in this cross-sectional study. An expert rheumatologist evaluated the myositis core set measures. Serum levels of cytokines and chemokines were quantified using the LEGENDplex Multi-Analyte Flow Assay Kit from BioLegend. The autoantibodies detection was carried out using the line-blot assay kit Euroline: Autoimmune Inflammatory Myopathies from EUROIMMUN. We found higher serum levels of IL-33, CXCL8, IL-6, IL-23, and IL-12p70 in seronegative patients. A multiple linear regression analysis revealed that MYOACT scores could be predicted by the increment of IL-23 and the decrement of CCL2, IL-10, and CXCL8 serum levels. These findings suggest that the immune response in seronegative myositis patients exhibits an IL-23-driven Th17 immune response. The relevance of this discovery lies in its potential therapeutic implications. Insights into the IL-23-driven Th17 immune response in seronegative patients highlight the potential for targeted therapies aimed at modulating Th17 activity. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition)
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Review

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20 pages, 1683 KB  
Review
Idiopathic Inflammatory Myopathies: Recent Evidence Linking Pathogenesis and Clinical Features
by Eunice Fragoso Martins, Carla Helena Cappello, Samuel Katsuyuki Shinjo, Simone Appenzeller and Jean Marcos de Souza
Int. J. Mol. Sci. 2025, 26(7), 3302; https://doi.org/10.3390/ijms26073302 - 2 Apr 2025
Viewed by 2488
Abstract
Idiopathic inflammatory myopathies are rare and complex representatives of systemic connective tissue diseases. Described initially as only two entities, recent advances in molecular and imaging techniques now divide them into many subtypes, each with unique pathogenesis and clinical phenotypes. Dermatomyositis and its juvenile [...] Read more.
Idiopathic inflammatory myopathies are rare and complex representatives of systemic connective tissue diseases. Described initially as only two entities, recent advances in molecular and imaging techniques now divide them into many subtypes, each with unique pathogenesis and clinical phenotypes. Dermatomyositis and its juvenile form are the most prevalent subtypes and are characterized by systemic vasculopathy and humoral autoimmunity. Genetic predisposition and environmental triggers initiate immune tolerance breakdown, leading to autoantibody production, complement activation, and tissue damage. Anti-synthetase syndrome primarily affects the lungs, where immune responses to aminoacyl-RNA synthetases drive vasculopathy, lung inflammation, and fibrosis. Immune-mediated necrotizing myopathies are muscle-specific, with autoantibodies inducing fiber necrosis and atrophy. Lastly, sporadic inclusion body myositis is a slowly progressive myopathy in which dysfunctional protein handling and autophagy are more important pathogenic elements than muscle inflammation itself. The expanding body of basic science evidence can be overwhelming, making it challenging to connect pathogenic mechanisms to clinical manifestations. This review aims to address this challenge by presenting recent insights into myositis pathogenesis from a practical perspective, reinforcing the links between basic science and clinical semiology. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition)
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Other

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10 pages, 984 KB  
Case Report
Life-Threatening Macrophage Activation Syndrome in Pregnancy: First Manifestation of SLE Induced by Parvovirus B19
by Aleksandra Plavsic, Rada Miskovic, Dragana Jovanovic, Uros Karic, Zikica Jovicic, Sara Radovic, Ana Drazic, Aleksandra Dasic and Snezana Arandjelovic
Int. J. Mol. Sci. 2025, 26(11), 5406; https://doi.org/10.3390/ijms26115406 - 4 Jun 2025
Viewed by 886
Abstract
Macrophage activation syndrome (MAS) is a complex, life-threatening, hyperinflammatory condition occurring as a form of hemophagocytic lymphohistiocytosis (HLH), commonly associated with several autoimmune and autoinflammatory diseases, and certain infections such as Parvovirus B19 (P19V). The onset of systemic lupus erythematosus (SLE) presenting as [...] Read more.
Macrophage activation syndrome (MAS) is a complex, life-threatening, hyperinflammatory condition occurring as a form of hemophagocytic lymphohistiocytosis (HLH), commonly associated with several autoimmune and autoinflammatory diseases, and certain infections such as Parvovirus B19 (P19V). The onset of systemic lupus erythematosus (SLE) presenting as MAS during pregnancy is uncommon, posing significant diagnostic and therapeutic challenges. We present a case of a 30-year-old woman at the 12th gestational week with fever, arthralgia, rash, cervical lymphadenopathy, cytopenia, and elevated liver enzyme. Bone marrow biopsy revealing hemophagocytosis, elevated ferritin and triglycerides, high interleukin-2, fever and cytopenia, confirmed the diagnosis of HLH. Further evaluation revealed the diagnosis of SLE. Treatment was initiated with intravenous immunoglobulin and corticosteroids. Given the deterioration in the patient’s clinical condition, a decision was made to terminate the pregnancy. She continued in the following months to receive SLE treatment with corticosteroids, cyclophosphamide, hydroxychloroquine, and later with mycophenolate mofetil due to the development of Class IV of lupus nephritis. P19V IgM antibodies were initially positive, later seroconverted to IgG, indicating that infection may have acted as a trigger for the onset of SLE and MAS development during pregnancy. The overlapping clinical features of P19V infection, SLE, and MAS pose significant diagnostic and therapeutic challenges. Early recognition and comprehensive diagnostic evaluation are crucial for the management of these conditions, especially during pregnancy, where both maternal outcomes are at risk. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Autoimmune Diseases—2nd Edition)
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