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Molecular and Cellular Mechanisms of Comorbidities in Rheumatic Diseases
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Molecular and Cellular Mechanisms of Comorbidities in Rheumatic 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: closed (20 November 2025) | Viewed by 2737

Special Issue Editor

Dr. Marino Paroli

E-Mail Website
Guest Editor
Division of Clinical Immunology, Department of Clinical, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy
Interests: inflammatory rheumatic diseases; autoimmunity; T-cell response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory and autoimmune rheumatic diseases place a great burden on patients and on health care systems. This is because of the disabling characteristics of these diseases, the high cost of new therapies, and the possible presence of co-morbidities that often require complex therapies. Therefore, this Special Issue aims to contribute original research and reviews on the molecular and cellular mechanisms of co-morbidities that often affect patients with rheumatic diseases. These may involve organs from different systems, such as those from cardiovascular, respiratory, gastrointestinal, nervous, renal, and skin systems. Scientific contributions are useful for managing patients better; indeed, facilitating early diagnoses is needed to avoid irreversible complications. This could also lead to savings for health care systems, as well as freeing up resources that can then be used to treat an increasing number of affected people.

Dr. Marino Paroli
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 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. 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

  • inflammatory and autoimmune rheumatic diseases
  • comorbidities
  • autoimmunity
  • T-cell response

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Published Papers (2 papers)

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Research

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14 pages, 1342 KB  
Article
BTLA-Expressing Memory B Cells Are Associated with Belimumab-Induced Improvement in Systemic Lupus Erythematosus
by Takuya Nishi, Kunihiro Hayakawa, Keigo Ikeda, Maki Fujishiro, Yuko Kataoka, Ken Yamaji, Kenji Takamori, Naoto Tamura, Iwao Sekigawa and Shinji Morimoto
Int. J. Mol. Sci. 2025, 26(23), 11323; https://doi.org/10.3390/ijms262311323 - 23 Nov 2025
Viewed by 342
Abstract
Belimumab, a fully humanized B cell-activating factor (BAFF)-targeting monoclonal antibody, inhibits autoreactive B cell survival and improves systemic lupus erythematosus (SLE) clinical outcomes. However, its administration criteria remain unclear. To establish a basis for defining these criteria, we characterized the immune cell subpopulation [...] Read more.
Belimumab, a fully humanized B cell-activating factor (BAFF)-targeting monoclonal antibody, inhibits autoreactive B cell survival and improves systemic lupus erythematosus (SLE) clinical outcomes. However, its administration criteria remain unclear. To establish a basis for defining these criteria, we characterized the immune cell subpopulation alterations post-belimumab treatment and elucidated the underlying mechanisms. We hypothesized that belimumab modulates specific cell subsets and investigated the post-therapy changes. Flow cytometry and correlation analysis revealed that the frequency of B- and T-lymphocyte attenuator (BTLA)high memory B cells in peripheral blood and clinical improvement after belimumab treatment. Western blotting analysis of healthy control B cells revealed that BTLA engagement suppressed Bruton tyrosine kinase and phospholipase C-gamma 2 phosphorylation, which was enhanced by B cell and BAFF receptor co-stimulation. BTLA-expressing memory B cells, which positively correlate with disease improvement, possibly contributed to SLE improvement via BTLA-mediated signaling that attenuated B cell- and BAFF receptor-induced intracellular pathways. To validate these findings, we plan to further assess the effects of belimumab on BTLA expression and B cell signaling pathways in treatment-naive patients with SLE by western blotting. Collectively, our results provide a novel foundation for establish appropriate belimumab administration criteria. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Comorbidities in Rheumatic Diseases)
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Review

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18 pages, 923 KB  
Review
Pathogenic Crosstalk Between the Peripheral and Central Nervous System in Rheumatic Diseases: Emerging Evidence and Clinical Implications
by Marino Paroli and Maria Isabella Sirinian
Int. J. Mol. Sci. 2025, 26(13), 6036; https://doi.org/10.3390/ijms26136036 - 24 Jun 2025
Viewed by 1615
Abstract
Systemic autoimmune rheumatic diseases (SARDs), such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS), are traditionally characterized by chronic inflammation and immune-mediated damage to joints and other tissues. However, many patients also experience symptoms such as widespread pain, persistent [...] Read more.
Systemic autoimmune rheumatic diseases (SARDs), such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS), are traditionally characterized by chronic inflammation and immune-mediated damage to joints and other tissues. However, many patients also experience symptoms such as widespread pain, persistent fatigue, cognitive dysfunction, and autonomic disturbances that cannot be attributed directly or entirely to peripheral inflammation or structural pathology. These conditions suggest the involvement of interactions between the nervous and immune systems, which probably include both peripheral and central components. This review summarizes the current knowledge of neurological and neuroimmune mechanisms that may contribute to these symptoms in SARDs. Glial cell activation and neuroinflammation within the central nervous system (CNS), small-fiber neuropathy (SFN) affecting peripheral nociceptive pathways, central pain sensitization, and autonomic nervous system dysfunction will be discussed. In addition, the role of molecular mediators, including cytokines, neuropeptides, and microRNAs, that could potentially modulate neuroimmune signaling will be highlighted. Integrating findings from pathology, immunology, and neuroscience, this review seeks to provide a useful framework for understanding neuroimmune dysregulation in SARDs. It also highlights the clinical relevance of these mechanisms and summarizes new directions for diagnosis and treatment. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Comorbidities in Rheumatic Diseases)
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