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Cells
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Advances in Cellular and Molecular Treatment of Autoimmune Diseases—Second Edition
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Advances in Cellular and Molecular Treatment of Autoimmune Diseases—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 October 2025) | Viewed by 2384

Special Issue Editors

Dr. Panagiotis Athanassiou

E-Mail Website
Guest Editor
Department of Rheumatology, St. Paul’s Hospital, Thessaloniki, Greece
Interests: rheumatoid arthritis; tumor necrosis factor; fatty acids; treatment; systemic lupus erythematosus
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Dimitrios P. Bogdanos

E-Mail Website
Guest Editor
Department of Internal Medicine and Autoimmune Rheumatic Diseases, School of Medicine, University of Thessaly, Larissa, Greece
Interests: autoimmunity; autoimmune diseases; diet; immunosuppression; immunoregulation; microbiome; nutrition; rheumatic diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Ifigenia Kostoglou-Athanassiou

E-Mail Website
Guest Editor
Department of Endocrinology, Asklepeion General Hospital, Athens, Greece
Interests: breast cancer; neuroendocrinology; melatonin; thyroid cancer; vitamin D; autoimmune diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Lately, there has been a world-wide increase in the prevalence and incidence of autoimmune diseases. Hence, extensive research is being conducted in order to identify the causes and risk factors of autoimmune diseases. Within the pathophysiology of autoimmune diseases, this has revealed the implication of various factors in their pathogenesis. The treatment of autoimmune diseases has been the subject of academic study in recent years. Corticosteroids may be applied as early treatment. Disease-modifying non-biologic drugs, such as methotrexate, leflunomide, sulfasalazine and hydroxychloroquine, have been used and may alter disease prognosis. Biologic agents targeting cellular and molecular targets have been introduced in the treatment of autoimmune diseases. They have induced disease remission and may have altered disease progression and long-term disease prognosis. Biologic agents may be used either intravenously or subcutaneously. However, they are costly. Therefore, biosimilars of these agents have been introduced in the treatment of autoimmune diseases. The concurrent application of non-biologic disease-modifying agents and biologics is being discussed. Currently, we have diverse effective agents targeting cellular and molecular targets in the treatment of autoimmune diseases. This has enabled the modification of treatment regimens to the needs of each individual patient.

Dr. Panagiotis Athanassiou
Prof. Dr. Dimitrios P. Bogdanos
Dr. Ifigenia Kostoglou-Athanassiou
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 250 words) can be sent to the Editorial Office for assessment.

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • disease activity
  • TNFa inhibitors
  • tocilizumab
  • infliximab
  • golimumab
  • etanercept
  • JAK inhibitors
  • cellular targets
  • molecular targets

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Related Special Issue

Published Papers (2 papers)

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Review

20 pages, 1206 KB  
Review
Linking AIM2 Inflammasome Activation, Mitochondrial Dysfunction and Chronic Inflammation in Ankylosing Spondylitis
by Catalina Alina Boengiu, Andreea-Lili Barbulescu, Cristiana Cerasella Dragomirescu, Ana-Maria Buga and Adina Andreea Mirea
Cells 2025, 14(23), 1923; https://doi.org/10.3390/cells14231923 - 3 Dec 2025
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Abstract
The absent in melanoma 2 (AIM2) inflammasome is a cytosolic DNA sensor that links genomic instability, mitochondrial dysfunction, and chronic inflammation. Unlike the nucleotide-binding domain, leucine-rich repeat (NLR) family pyrin domain-containing protein 3 (NLRP3) inflammasome, AIM2 is activated directly by double-stranded Deoxyribonucleic Acid [...] Read more.
The absent in melanoma 2 (AIM2) inflammasome is a cytosolic DNA sensor that links genomic instability, mitochondrial dysfunction, and chronic inflammation. Unlike the nucleotide-binding domain, leucine-rich repeat (NLR) family pyrin domain-containing protein 3 (NLRP3) inflammasome, AIM2 is activated directly by double-stranded Deoxyribonucleic Acid (dsDNA), including mitochondrial DNA (mtDNA) released under stress conditions. This positions AIM2 at the intersection of oxidative stress, impaired mitophagy, and innate immune dysregulation. Current therapies for ankylosis spondylitis (AS), such as anti-tumor necrosis factor (TNF), anti-interleukin 17 (IL-17), and Janus kinase (JAK) inhibitors, improve clinical outcomes; however, they do not address upstream mitochondrial dysfunction or DNA-driven inflammasome activation. By contrast, other inflammasomes, such as AIM2, remain comparatively less studied. Since autoimmune diseases, including AS, are frequently accompanied by uncontrolled innate immune responses to self-DNA, these findings provide a framework for comprehending the mechanisms of AIM2 activation and its interaction with inflammation, mitophagy, and oxidative stress. Here, we review the current evidence on AIM2 inflammasome involvement in AS pathogenesis and its potential as a therapeutic target. This approach offers new insight into disease control through re-establishing the balance between mitochondrial dysfunction and autoimmunity. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Treatment of Autoimmune Diseases—Second Edition)
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16 pages, 701 KB  
Review
The Autoimmune Gastritis Puzzle: Emerging Cellular Crosstalk and Molecular Pathways Driving Parietal Cell Loss and ECL Cell Hyperplasia
by Sara Massironi, Elena Oriani, Giuseppe Dell’Anna, Silvio Danese and Federica Facciotti
Cells 2025, 14(20), 1576; https://doi.org/10.3390/cells14201576 - 10 Oct 2025
Cited by 1 | Viewed by 1682
Abstract
Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by progressive destruction of gastric parietal cells driven by autoreactive CD4+ T-cells, epithelial stress pathways, and microbial factors. Parietal cell loss results in achlorhydria, intrinsic factor deficiency, and vitamin B12 malabsorption, ultimately [...] Read more.
Autoimmune gastritis (AIG) is a chronic, organ-specific autoimmune disease characterized by progressive destruction of gastric parietal cells driven by autoreactive CD4+ T-cells, epithelial stress pathways, and microbial factors. Parietal cell loss results in achlorhydria, intrinsic factor deficiency, and vitamin B12 malabsorption, ultimately leading to pernicious anemia. Compensatory hypergastrinemia promotes enterochromaffin-like (ECL) cell hyperplasia and contributes to the development of type 1 gastric neuroendocrine neoplasms (gNENs). These clinical consequences are well recognized, yet the cellular and molecular mechanisms driving mucosal atrophy and neoplastic transformation remain incompletely defined. Recent advances highlight the role of endoplasmic reticulum stress, impaired autophagy, innate immune effectors, and dysbiosis in perpetuating inflammation and epithelial injury. The frequent coexistence of AIG with other autoimmune disorders further adds to its clinical complexity. Therapeutic options remain limited, spanning vitamin B12 replacement and endoscopic management to emerging targeted approaches. Netazepide, a gastrin/CCK2 receptor antagonist, is the only agent tested in clinical trials, whereas interventions targeting ER stress, autophagy, immune tolerance, or microbiome composition are still in the preclinical stage. Clarifying these mechanisms is crucial to improve biomarker development, optimize surveillance, and identify targeted therapies to prevent neoplastic transformation. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Treatment of Autoimmune Diseases—Second Edition)
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