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Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition
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Autoimmune Diseases: A Swing Dance of Immune Cells, 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: closed (20 April 2025) | Viewed by 23303

Special Issue Editor

Prof. Dr. Balik Dzhambazov

E-Mail Website
Guest Editor
Faculty of Biology, Plovdiv University “Paisii Hilendarski”, 24 Tsar Assen Str., 4000 Plovdiv, Bulgaria
Interests: cell biology; immunology; immunomodulation; biomarkers; autoimmune diseases; allergy; cytotoxicity; anticancer activity; natural products; probiotics; prebiotics; nanoparticles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The human body constantly interacts with other organisms and with the environment. Such interactions allow the body to recognize beneficial influences from harmful influences, as well as what is its own and what is foreign. This is achieved through the immune system, which is a complex network of specialized cells and organs. Therefore, immune system cells are in a continuous "dance with different partners". The frequent "switching of partners" can lead to the immune system being unable to distinguish between self and non-self, which can initiate the development of autoimmune diseases. There are more than 80 known autoimmune diseases, some of which are more common and well studied (such as rheumatoid arthritis, multiple sclerosis, type 1 diabetes, and lupus), although others are rare. Interestingly, the etiology of most autoimmune diseases remains a mystery.

In this Special Issue, the key word is "change", i.e., changes in key molecules during disease-versus-normal states. We discuss changes in antigens, molecular interactions, antibody production, cell signaling, or tissue/organ structures which are associated with the initiation, development, or progression of autoimmune diseases. The development of therapeutic agents that target signaling pathways and lead to changes in T-cell or humoral immune responses will also be considered.

More published papers could be found in the closed Special Issue: Autoimmune Diseases: A Swing Dance of the Immune Cells.

Prof. Dr. Balik Dzhambazov
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. 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

  • autoimmune diseases
  • antigens/autoantigens
  • post-translational modifications
  • antigen processing and presentation
  • shared epitopes
  • molecular mimicry
  • autoantibodies
  • immune signaling
  • animal models
  • therapeutic agents

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Published Papers (5 papers)

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Research

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24 pages, 9276 KiB  
Article
Impact of Neuron-Derived HGF on c-Met and KAI-1 in CNS Glial Cells: Implications for Multiple Sclerosis Pathology
by Takuma Takano, Chie Takano, Hiroshi Funakoshi and Yoshio Bando
Int. J. Mol. Sci. 2024, 25(20), 11261; https://doi.org/10.3390/ijms252011261 - 19 Oct 2024
Cited by 1 | Viewed by 1270
Abstract
Demyelination and axonal degeneration are fundamental pathological characteristics of multiple sclerosis (MS), an inflammatory disease of the central nervous system (CNS). Although the molecular mechanisms driving these processes are not fully understood, hepatocyte growth factor (HGF) has emerged as a potential regulator of [...] Read more.
Demyelination and axonal degeneration are fundamental pathological characteristics of multiple sclerosis (MS), an inflammatory disease of the central nervous system (CNS). Although the molecular mechanisms driving these processes are not fully understood, hepatocyte growth factor (HGF) has emerged as a potential regulator of neuroinflammation and tissue protection in MS. Elevated HGF levels have been reported in MS patients receiving immunomodulatory therapy, indicating its relevance in disease modulation. This study investigated HGF’s neuroprotective effects using transgenic mice that overexpressed HGF. The experimental autoimmune encephalomyelitis (EAE) model, which mimics MS pathology, was employed to assess demyelination and axonal damage in the CNS. HGF transgenic mice showed delayed EAE progression, with reduced CNS inflammation, decreased demyelination, and limited axonal degeneration. Scanning electron microscopy confirmed the preservation of myelin and axonal integrity in these mice. In addition, we explored HGF’s effects using a cuprizone-induced demyelination model, which operates independently of the immune system. HGF transgenic mice exhibited significant protection against demyelination in this model as well. We also investigated the expression of key HGF receptors, particularly c-Met and KAI-1. While c-Met, which is associated with increased inflammation, was upregulated in EAE, its expression was significantly reduced in HGF transgenic mice, correlating with decreased neuroinflammation. Conversely, KAI-1, which has been linked to axonal protection and stability, showed enhanced expression in HGF transgenic mice, suggesting a protective mechanism against axonal degeneration. These findings underscore HGF’s potential in preserving CNS structure and function, suggesting it may be a promising therapeutic target for MS, offering new hope for mitigating disease progression and enhancing neuroprotection. Full article
(This article belongs to the Special Issue Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition)
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10 pages, 5123 KiB  
Communication
Raman Spectroscopy of Optically Trapped Living Human T Cell Subsets and Monocytes
by Martin Nötzel, Maria Mahamid, Romy Kronstein-Wiedemann, Tjalf Ziemssen and Katja Akgün
Int. J. Mol. Sci. 2024, 25(17), 9557; https://doi.org/10.3390/ijms25179557 - 3 Sep 2024
Cited by 1 | Viewed by 1294
Abstract
In recent years, Raman spectroscopy has garnered growing interest in the field of biomedical research. It offers a non-invasive and label-free approach to defining the molecular fingerprint of immune cells. We utilized Raman spectroscopy on optically trapped immune cells to investigate their molecular [...] Read more.
In recent years, Raman spectroscopy has garnered growing interest in the field of biomedical research. It offers a non-invasive and label-free approach to defining the molecular fingerprint of immune cells. We utilized Raman spectroscopy on optically trapped immune cells to investigate their molecular compositions. While numerous immune cell types have been studied in the past, the characterization of living human CD3/CD28-stimulated T cell subsets remains incomplete. In this study, we demonstrate the capability of Raman spectroscopy to readily distinguish between naïve and stimulated CD4 and CD8 cells. Additionally, we compared these cells with monocytes and discovered remarkable similarities between stimulated T cells and monocytes. This paper contributes to expanding our knowledge of Raman spectroscopy of immune cells and serves as a launching point for future clinical applications. Full article
(This article belongs to the Special Issue Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition)
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21 pages, 5709 KiB  
Article
Study on the Treatment of ITP Mice with IVIG Sourced from Distinct Sex-Special Plasma (DSP-IVIG)
by Wei Zhang, Xin Yuan, Zongkui Wang, Jixuan Xu, Shengliang Ye, Peng Jiang, Xi Du, Fengjuan Liu, Fangzhao Lin, Rong Zhang, Li Ma and Changqing Li
Int. J. Mol. Sci. 2023, 24(21), 15993; https://doi.org/10.3390/ijms242115993 - 6 Nov 2023
Cited by 3 | Viewed by 2656
Abstract
Intravenous immunoglobulin (IVIG) is a first-line drug prepared from human plasma for the treatment of autoimmune diseases (AIDs), especially immune thrombocytopenia (ITP). Significant differences exist in protein types and expression levels between male and female plasma, and the prevalence of autoimmune diseases varies [...] Read more.
Intravenous immunoglobulin (IVIG) is a first-line drug prepared from human plasma for the treatment of autoimmune diseases (AIDs), especially immune thrombocytopenia (ITP). Significant differences exist in protein types and expression levels between male and female plasma, and the prevalence of autoimmune diseases varies between sexes. The present study seeks to explore potential variations in IVIG sourced from distinct sex-specific plasma (DSP-IVIG), including IVIG sourced from female plasma (F-IVIG), IVIG sourced from male plasma (M-IVIG), and IVIG sourced from a blend of male and female plasma (Mix-IVIG). To address this question, we used an ITP mouse model and a monocyte–macrophage inflammation model treated with DSP IVIG. The analysis of proteomics in mice suggested that the pathogenesis and treatment of ITP may involve FcγRs mediated phagocytosis, apoptosis, Th17, cytokines, chemokines, and more. Key indicators, including the mouse spleen index, CD16+ macrophages, M1, M2, IL-6, IL-27, and IL-13, all indicated that the efficacy in improving ITP was highest for M-IVIG. Subsequent cell experiments revealed that M-IVIG exhibited a more potent ability to inhibit monocyte phagocytosis. It induced more necrotic M2 cells and fewer viable M2, resulting in weaker M2 phagocytosis. M-IVIG also demonstrated superiority in the downregulation of surface makers CD36, CD68, and CD16 on M1 macrophages, a weaker capacity to activate complement, and a stronger binding ability to FcγRs on the THP-1 surface. In summary, DSP-IVIG effectively mitigated inflammation in ITP mice and monocytes and macrophages. However, M-IVIG exhibited advantages in improving the spleen index, regulating the number and typing of M1 and M2 macrophages, and inhibiting macrophage-mediated inflammation compared to F-IVIG and Mix-IVIG. Full article
(This article belongs to the Special Issue Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition)
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Review

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20 pages, 1407 KiB  
Review
The Lung in Rheumatoid Arthritis—Friend or Enemy?
by Maria-Luciana Anton, Anca Cardoneanu, Alexandra Maria Burlui, Ioana Ruxandra Mihai, Patricia Richter, Ioana Bratoiu, Luana Andreea Macovei and Elena Rezus
Int. J. Mol. Sci. 2024, 25(12), 6460; https://doi.org/10.3390/ijms25126460 - 12 Jun 2024
Cited by 7 | Viewed by 2416
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune condition frequently found in rheumatological patients that sometimes raises diagnosis and management problems. The pathogenesis of the disease is complex and involves the activation of many cells and intracellular signaling pathways, ultimately leading to the activation [...] Read more.
Rheumatoid arthritis (RA) is a chronic autoimmune condition frequently found in rheumatological patients that sometimes raises diagnosis and management problems. The pathogenesis of the disease is complex and involves the activation of many cells and intracellular signaling pathways, ultimately leading to the activation of the innate and acquired immune system and producing extensive tissue damage. Along with joint involvement, RA can have numerous extra-articular manifestations (EAMs), among which lung damage, especially interstitial lung disease (ILD), negatively influences the evolution and survival of these patients. Although there are more and more RA-ILD cases, the pathogenesis is incompletely understood. In terms of genetic predisposition, external environmental factors act and subsequently determine the activation of immune system cells such as macrophages, neutrophils, B and T lymphocytes, fibroblasts, and dendritic cells. These, in turn, show the ability to secrete molecules with a proinflammatory role (cytokines, chemokines, growth factors) that will produce important visceral injuries, including pulmonary changes. Currently, there is new evidence that supports the initiation of the systemic immune response at the level of pulmonary mucosa where the citrullination process occurs, whereby the autoantibodies subsequently migrate from the lung to the synovial membrane. The aim of this paper is to provide current data regarding the pathogenesis of RA-associated ILD, starting from environmental triggers and reaching the cellular, humoral, and molecular changes involved in the onset of the disease. Full article
(This article belongs to the Special Issue Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition)
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17 pages, 374 KiB  
Review
Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management
by Melika Loriamini, Christine Cserti-Gazdewich and Donald R. Branch
Int. J. Mol. Sci. 2024, 25(8), 4296; https://doi.org/10.3390/ijms25084296 - 12 Apr 2024
Cited by 13 | Viewed by 14583
Abstract
Autoimmune hemolytic anemias (AIHAs) are conditions involving the production of antibodies against one’s own red blood cells (RBCs). These can be primary with unknown cause or secondary (by association with diseases or infections). There are several different categories of AIHAs recognized according to [...] Read more.
Autoimmune hemolytic anemias (AIHAs) are conditions involving the production of antibodies against one’s own red blood cells (RBCs). These can be primary with unknown cause or secondary (by association with diseases or infections). There are several different categories of AIHAs recognized according to their features in the direct antiglobulin test (DAT). (1) Warm-antibody AIHA (wAIHA) exhibits a pan-reactive IgG autoantibody recognizing a portion of band 3 (wherein the DAT may be positive with IgG, C3d or both). Treatment involves glucocorticoids and steroid-sparing agents and may consider IVIG or monoclonal antibodies to CD20, CD38 or C1q. (2) Cold-antibody AIHA due to IgMs range from cold agglutinin syndrome (CAS) to cold agglutin disease (CAD). These are typically specific to the Ii blood group system, with the former (CAS) being polyclonal and the latter (CAD) being a more severe and monoclonal entity. The DAT in either case is positive only with C3d. Foundationally, the patient is kept warm, though treatment for significant complement-related outcomes may, therefore, capitalize on monoclonal options against C1q or C5. (3) Mixed AIHA, also called combined cold and warm AIHA, has a DAT positive for both IgG and C3d, with treatment approaches inclusive of those appropriate for wAIHA and cold AIHA. (4) Paroxysmal cold hemoglobinuria (PCH), also termed Donath–Landsteiner test-positive AIHA, has a DAT positive only for C3d, driven upstream by a biphasic cold-reactive IgG antibody recruiting complement. Although usually self-remitting, management may consider monoclonal antibodies to C1q or C5. (5) Direct antiglobulin test-negative AIHA (DAT-neg AIHA), due to IgG antibody below detection thresholds in the DAT, or by non-detected IgM or IgA antibodies, is managed as wAIHA. (6) Drug-induced immune hemolytic anemia (DIIHA) appears as wAIHA with DAT IgG and/or C3d. Some cases may resolve after ceasing the instigating drug. (7) Passenger lymphocyte syndrome, found after transplantation, is caused by B-cells transferred from an antigen-negative donor whose antibodies react with a recipient who produces antigen-positive RBCs. This comprehensive review will discuss in detail each of these AIHAs and provide information on diagnosis, pathophysiology and treatment modalities. Full article
(This article belongs to the Special Issue Autoimmune Diseases: A Swing Dance of Immune Cells, 2nd Edition)
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