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Cellular and Molecular Mechanisms of Autoimmune Disorders
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Cellular and Molecular Mechanisms of Autoimmune Disorders

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 7869

Special Issue Editor

Prof. Dr. Ritva Tikkanen

E-Mail Website
Guest Editor
Institute of Biochemistry, Medical Faculty, Justus-Liebig University of Giessen, Friedrichstrasse 24, D-35392 Giessen, Germany
Interests: lysosomal storage disorders; vesicular trafficking; endosomal sorting; lysosome biogenesis; mitochondrial diseases; autoimmune disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases are characterized by an impaired self-tolerance and by pathogenic antibodies against normal tissue proteins. These autoantibodies can directly damage their target tissues, or they can induce aberrant downstream effects, e.g., by stimulating signaling molecules. Various tissues such as the epidermis, thyroid, neuromuscular junction, myelinated nerves or the pancreas can be targets of such autoantibodies. Profound inflammation can be a result of autoimmunity, and the first line of treatment has traditionally been anti-inflammatory therapy with corticosteroids. However, more targeted therapies have started to emerge as our understanding of the molecular and cellular pathomechanisms is growing.

The purpose of this Special Issue is to highlight novel aspects of the cellular and molecular mechanisms of human autoimmune diseases. We encourage the submission of review articles and original research papers of any length. Our aim is to provide a comprehensive update on the pathomechanisms of autoimmune diseases at the cellular and molecular level.

Prof. Dr. Ritva Tikkanen
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
  • self-tolerance
  • immune cells
  • autoantibodies
  • autoantigens
  • pathomechanisms

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Published Papers (3 papers)

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Research

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16 pages, 2849 KiB  
Article
An In-Depth Exploration of the Autoantibody Immune Profile in ME/CFS Using Novel Antigen Profiling Techniques
by Arnaud Germain, Jillian R. Jaycox, Christopher J. Emig, Aaron M. Ring and Maureen R. Hanson
Int. J. Mol. Sci. 2025, 26(6), 2799; https://doi.org/10.3390/ijms26062799 - 20 Mar 2025
Viewed by 4064
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by serious physical and cognitive impairments. Recent research underscores the role of immune dysfunction, including the role of autoantibodies, in ME/CFS pathophysiology. Expanding on previous studies, we analyzed 7542 antibody–antigen interactions in ME/CFS [...] Read more.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by serious physical and cognitive impairments. Recent research underscores the role of immune dysfunction, including the role of autoantibodies, in ME/CFS pathophysiology. Expanding on previous studies, we analyzed 7542 antibody–antigen interactions in ME/CFS patients using two advanced platforms: a 1134 autoantibody Luminex panel from Oncimmune and Augmenta Bioworks, along with Rapid Extracellular Antigen Profiling (REAP), a validated high-throughput method that measures autoantibody reactivity against 6183 extracellular human proteins and 225 human viral pathogen proteins. Unlike earlier reports, our analysis of 172 participants revealed no significant differences in autoantibody reactivities between ME/CFS patients and controls, including against GPCRs such as β-adrenergic receptors. However, subtle trends in autoantibody ratios between male and female ME/CFS subgroups, along with patterns of herpesvirus reactivation, suggest the need for broader and more detailed exploration. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Autoimmune Disorders)
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19 pages, 2334 KiB  
Article
Glycosylation Regulation by TMEM230 in Aging and Autoimmunity
by Eleonora Piscitelli, Edoardo Abeni, Cristiana Balbino, Elena Angeli, Cinzia Cocola, Paride Pelucchi, Mira Palizban, Alberto Diaspro, Martin Götte, Ileana Zucchi and Rolland A. Reinbold
Int. J. Mol. Sci. 2025, 26(6), 2412; https://doi.org/10.3390/ijms26062412 - 7 Mar 2025
Viewed by 722
Abstract
Aging is often a choice between developing cancer or autoimmune disorders, often due in part to loss of self-tolerance or loss of immunological recognition of rogue-acting tumor cells. Self-tolerance and cell recognition by the immune system are processes very much dependent on the [...] Read more.
Aging is often a choice between developing cancer or autoimmune disorders, often due in part to loss of self-tolerance or loss of immunological recognition of rogue-acting tumor cells. Self-tolerance and cell recognition by the immune system are processes very much dependent on the specific signatures of glycans and glycosylated factors present on the cell plasma membrane or in the stromal components of tissue. Glycosylated factors are generated in nearly innumerable variations in nature, allowing for the immensely diverse role of these factors in aging and flexibility necessary for cellular interactions in tissue functionality. In previous studies, we showed that differential expression of TMEM230, an endoplasmic reticulum (ER) protein was associated with specific signatures of enzymes regulating glycan synthesis and processing and glycosylation in rheumatoid arthritis synovial tissue using single-cell transcript sequencing. In this current study, we characterize the genes and pathways co-modulated in all cell types of the synovial tissue with the enzymes regulating glycan synthesis and processing, as well as glycosylation. Genes and biological and molecular pathways associated with hallmarks of aging were in mitochondria-dependent oxidative phosphorylation and reactive oxygen species synthesis, ER-dependent stress and unfolded protein response, DNA repair (UV response and P53 signaling pathways), and senescence, glycolysis and apoptosis regulation through PI3K-AKT-mTOR signaling have been shown to play important roles in aging or neurodegeneration (such as Parkinson’s and Alzheimer’s disease). We propose that the downregulation of TMEM230 and RNASET2 may represent a paradigm for the study of age-dependent autoimmune disorders due to their role in regulating glycosylation, unfolded protein response, and PI3K-AKT-mTOR signaling. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Autoimmune Disorders)
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Review

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29 pages, 3375 KiB  
Review
Lymphocytes Change Their Phenotype and Function in Systemic Lupus Erythematosus and Lupus Nephritis
by Eleni Moysidou, Michalis Christodoulou, Georgios Lioulios, Stamatia Stai, Theodoros Karamitsos, Theodoros Dimitroulas, Asimina Fylaktou and Maria Stangou
Int. J. Mol. Sci. 2024, 25(20), 10905; https://doi.org/10.3390/ijms252010905 - 10 Oct 2024
Cited by 3 | Viewed by 2399
Abstract
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, characterized by considerable changes in peripheral lymphocyte structure and function, that plays a critical role in commencing and reviving the inflammatory and immune signaling pathways. In healthy individuals, B lymphocytes have a major role [...] Read more.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, characterized by considerable changes in peripheral lymphocyte structure and function, that plays a critical role in commencing and reviving the inflammatory and immune signaling pathways. In healthy individuals, B lymphocytes have a major role in guiding and directing defense mechanisms against pathogens. Certain changes in B lymphocyte phenotype, including alterations in surface and endosomal receptors, occur in the presence of SLE and lead to dysregulation of peripheral B lymphocyte subpopulations. Functional changes are characterized by loss of self-tolerance, intra- and extrafollicular activation, and increased cytokine and autoantibody production. T lymphocytes seem to have a supporting, rather than a leading, role in the disease pathogenesis. Substantial aberrations in peripheral T lymphocyte subsets are evident, and include a reduction of cytotoxic, regulatory, and advanced differentiated subtypes, together with an increase of activated and autoreactive forms and abnormalities in follicular T cells. Up-regulated subpopulations, such as central and effector memory T cells, produce pre-inflammatory cytokines, activate B lymphocytes, and stimulate cell signaling pathways. This review explores the pivotal roles of B and T lymphocytes in the pathogenesis of SLE and Lupus Nephritis, emphasizing the multifaceted mechanisms and interactions and their phenotypic and functional dysregulations. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Autoimmune Disorders)
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