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Mechanisms of Immune Tolerance and Autoimmune Diseases
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Mechanisms of Immune Tolerance and Autoimmune Diseases

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 October 2025 | Viewed by 14443

Special Issue Editors

Prof. Dr. Marcos López Hoyos

E-Mail Website
Guest Editor
1. Institute for Research Marqués de Valdecilla (IDIVAL), 39011 Santander, Spain
2. Immunology Department, Marqués de Valdecilla University Hospital, 39008 Santander, Spain
3. Molecular Biology Department, University of Cantabria, 39011 Santander, Spain
4. National Microbiology Center, National Institute of Health Carlos III, 28220 Madrid, Spain
5. Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
Interests: immunology; autoimmunity; transplantation; tolerance; human pathology; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Jordi Ochando

E-Mail Website
Guest Editor
Instituto de Salud Carlos III, Majadahonda, 28029 Madrid, Spain
Interests: trained immunity; immune tolerance; organ transplantation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The field of immunological tolerance and the induction of autoimmune diseases has started focusing on the role of the adaptative immune response and how the failure of central and peripheral tolerance could induce autoimmunity. In the last decade, increasing attention has been paid to the ways in which innate immunity and the cellular participants in inflammation might be implicated in these diseases. Therefore, several new autoinflammatory diseases have been described using the genetic data associated with functional consequences. Through the study of the genetic, phenotypic, metabolic and functional mechanisms involved in these immune-mediated diseases, novel diagnostic and therapeutic approaches have been developed. Furthermore, there is continuum with no clear border between autoinflammatory and autoimmune disease. This Special Issue specifically welcomes the submission of studies that focus on the basic mechanisms underlying the production of autoimmune and autoinflammatory diseases, in addition to translational studies.

Prof. Dr. Marcos López Hoyos
Dr. Jordi Ochando
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

  • immunological tolerance
  • autoimmune diseases
  • autoinflammatory diseases
  • inflammation
  • immune-mediated diseases

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Published Papers (3 papers)

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Research

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14 pages, 1799 KiB  
Article
Breaking the Triad: Immune Tolerance Induction Without Antigen Co-Presentation via Tim Agonist for the Treatment of Autoimmune Diseases
by Basel Karzoun, Abdulraouf Ramadan, Saleh Allababidi and Anas M. Fathallah
Int. J. Mol. Sci. 2025, 26(12), 5531; https://doi.org/10.3390/ijms26125531 - 10 Jun 2025
Viewed by 229
Abstract
Autoimmune diseases such as multiple sclerosis (MS) are characterized by a loss of self-tolerance, driven by diminished regulatory T cell (Treg) function and elevated Th1/Th17 responses. Existing therapies broadly suppress the immune system without correcting this imbalance, often leading to adverse effects. LPX3, [...] Read more.
Autoimmune diseases such as multiple sclerosis (MS) are characterized by a loss of self-tolerance, driven by diminished regulatory T cell (Treg) function and elevated Th1/Th17 responses. Existing therapies broadly suppress the immune system without correcting this imbalance, often leading to adverse effects. LPX3, a novel small-molecule T cell immunoglobulin and mucin domain-containing 3 and 4 (Tim-3/4) receptor agonist, was developed to restore immune tolerance via Treg induction. In this study, LPX3 was formulated into a liposomal oral delivery system, enabling efficient uptake through the gastrointestinal tract and lymphatic targeting. In vitro and in vivo analyses confirmed LPX3’s ability to expand CD4+Foxp3+ Tregs in a dose-dependent manner. In a MOG-induced experimental autoimmune encephalomyelitis (EAE) mouse model of MS, both prophylactic and therapeutic oral administration of LPX3 significantly delayed disease onset, reduced symptom severity, and improved survival. Importantly, efficacy was achieved without antigen co-delivery, indicating an antigen-independent mechanism of immune modulation. LPX3 liposomes showed deep lymph node penetration and colocalization with immune cells, supporting its functional delivery to key immunological sites. These findings suggest LPX3 is a promising candidate for treating autoimmune diseases by re-establishing immune regulation through oral, antigen-agnostic tolerance induction. Full article
(This article belongs to the Special Issue Mechanisms of Immune Tolerance and Autoimmune Diseases)
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13 pages, 2024 KiB  
Article
Changes in NK Cells and Exhausted Th Cell Phenotype in RA Patients Treated with Janus Kinase Inhibitors: Implications for Adverse Effects
by Juan José Fernández-Cabero, Carmen Lasa-Teja, David San Segundo, Alejandra Comins-Boo, Juan Irure-Ventura, David Walias Rivera, Jose Luis Martín-Varillas, Cristina Mata, Montserrat Santos, Elena Aurrecoechea, Ricardo Blanco and Marcos López-Hoyos
Int. J. Mol. Sci. 2025, 26(11), 5160; https://doi.org/10.3390/ijms26115160 - 28 May 2025
Viewed by 310
Abstract
Recent concerns regarding the safety of Janus kinase inhibitors (JAKis) have prompted investigation into their impact on immune cell subsets in rheumatoid arthritis (RA) patients. This study aims to analyse alterations in immune cell populations induced by JAKis that may contribute to adverse [...] Read more.
Recent concerns regarding the safety of Janus kinase inhibitors (JAKis) have prompted investigation into their impact on immune cell subsets in rheumatoid arthritis (RA) patients. This study aims to analyse alterations in immune cell populations induced by JAKis that may contribute to adverse events, such as infections or malignancies. This study included 78 RA patients meeting ACR/EULAR criteria with an established treatment with JAKis (tofacitinib, baricitinib, upadacitinib, or filgotinib), 20 healthy donors, and 20 RA patients treated with biological disease-modifying antirheumatic drugs (bDMARDs). Peripheral blood mononuclear cells (PBMCs) were immunophenotyped directly after isolation using multiparametric flow cytometry to characterise innate and adaptive immune-cell subsets. JAKi-treated patients showed a significant reduction in cytotoxic NK Dim (CD3−CD56+CD16+) cells and in the percentage of NK Dim cells expressing the activation marker Nkp30. In CD4+ T cells, the percentage of Th17 (CD3+CD4+CD45RA+CCR6+CXCR3−), Th1-17 (CD3+CD4+CD45RA+CCR6+CXCR3+), and central memory (CM, CD3+CD4+CD45RA+CD62L+) cells was lower in the JAKi group, while effector memory (EM, CD3+CD4+CD45RA−CD62L−) and terminally differentiated CD45RA (TEMRA, CD3+CD4+CD45RA+CD62L−) T helper cells were increased compared to healthy and bDMARD-treated controls. The reduction in NK Dim and Th1-17 cells and the increase in exhausted Th subsets suggest a potential compromise in antiviral immunity and balanced immune responses in JAKi-treated RA patients. These alterations may contribute to an increased risk of infections or malignancies. Full article
(This article belongs to the Special Issue Mechanisms of Immune Tolerance and Autoimmune Diseases)
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Review

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29 pages, 1678 KiB  
Review
Understanding Autoimmunity: Mechanisms, Predisposing Factors, and Cytokine Therapies
by Farzana Yasmeen, Rameez Hassan Pirzada, Bilal Ahmad, Bogeum Choi and Sangdun Choi
Int. J. Mol. Sci. 2024, 25(14), 7666; https://doi.org/10.3390/ijms25147666 - 12 Jul 2024
Cited by 25 | Viewed by 13160
Abstract
Autoimmunity refers to an organism’s immune response against its own healthy cells, tissues, or components, potentially leading to irreversible damage to vital organs. Central and peripheral tolerance mechanisms play crucial roles in preventing autoimmunity by eliminating self-reactive T and B cells. The disruption [...] Read more.
Autoimmunity refers to an organism’s immune response against its own healthy cells, tissues, or components, potentially leading to irreversible damage to vital organs. Central and peripheral tolerance mechanisms play crucial roles in preventing autoimmunity by eliminating self-reactive T and B cells. The disruption of immunological tolerance, characterized by the failure of these mechanisms, results in the aberrant activation of autoreactive lymphocytes that target self-tissues, culminating in the pathogenesis of autoimmune disorders. Genetic predispositions, environmental exposures, and immunoregulatory disturbances synergistically contribute to the susceptibility and initiation of autoimmune pathologies. Within the realm of immune therapies for autoimmune diseases, cytokine therapies have emerged as a specialized strategy, targeting cytokine-mediated regulatory pathways to rectify immunological imbalances. Proinflammatory cytokines are key players in inducing and propagating autoimmune inflammation, highlighting the potential of cytokine therapies in managing autoimmune conditions. This review discusses the etiology of autoimmune diseases, current therapeutic approaches, and prospects for future drug design. Full article
(This article belongs to the Special Issue Mechanisms of Immune Tolerance and Autoimmune Diseases)
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