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Treatment Strategies and Immune Responses in Rheumatic Diseases
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Treatment Strategies and Immune Responses in Rheumatic Diseases

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: 30 April 2025 | Viewed by 3175

Special Issue Editor

Dr. Rita Aguiar Moura

E-Mail Website1 Website2
Guest Editor
Instituto de Medicina Molecular João Lobo Antunes, Lisbon, Portugal
Interests: autoimmune diseases; immunopathogenesis; B cells; T cells; autoantibodies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Rheumatic diseases are chronic inflammatory immune-mediated disorders that may affect the joints, muscles, and bones and that exhibit systemic and/or organ-specific involvement. These conditions can have a major impact on patients’ quality of life, society more broadly, and can represent an economic burden. Therefore, facilitating early diagnosis and providing adequate treatment are fundamental for effective disease management.

Treatment options in rheumatic disorders include the use of non-steroid anti-inflammatory drugs (NSAIDs), corticosteroids, synthetic and biological disease-modifying anti-rheumatic drugs (DMARDs). Synthetic DMARDs can be further classified as conventional DMARDs, such as methotrexate, or as targeted DMARDs, such as janus kinase (JAK)-inhibitors. Biological DMARDs include tumor necrosis factor (TNF)-inhibitors; the interleukin (IL)-6 receptor antagonist tocilizumab; the T-cell co-stimulation modulator abatacept; and the B-cell depleting agent rituximab.

Despite the progresses achieved in recent decades and the development of novel treatment strategies to effectively stop or attenuate the progression of rheumatic diseases, not all patients reach sustained remission and refractory disease remains a significant challenge.

The aim of this Special Issue is to collect original research articles and/or reviews that focus on the impact of treatment management and immune responses in rheumatic diseases and novel approaches in precision medicine.

Dr. Rita Aguiar Moura
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. Diseases is an international peer-reviewed open access monthly 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 1800 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

  • rheumatic diseases
  • disease-modifying anti-rheumatic drugs (DMARDs)
  • immune responses
  • precision medicine

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Published Papers (3 papers)

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Research

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20 pages, 4470 KiB  
Article
Artemisia pallens W. Attenuates Inflammation and Oxidative Stress in Freund’s Complete Adjuvant-Induced Rheumatoid Arthritis in Wistar Rats
by Tasneem Ahmad, Parag Kadam, Gopal Bhiyani, Hasan Ali, Md. Akbar, Mohd Usman Mohd Siddique and Mudassar Shahid
Diseases 2024, 12(10), 230; https://doi.org/10.3390/diseases12100230 - 29 Sep 2024
Viewed by 805
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease that causes distinctive inflammatory symptoms and affects over 21 million people worldwide. RA is characterized by severe discomfort, swelling, and degradation of the bone and cartilage, further impairing joint function. The current study investigates the antiarthritic [...] Read more.
Rheumatoid arthritis (RA) is an autoimmune disease that causes distinctive inflammatory symptoms and affects over 21 million people worldwide. RA is characterized by severe discomfort, swelling, and degradation of the bone and cartilage, further impairing joint function. The current study investigates the antiarthritic effect of a methanolic extract of Artemisia pallens (methanolic extract of A. pallens, MEAP), an aromatic herb. Artemisinin content (% per dry weight of the plant) was estimated using a UV Vis spectrophotometer. In the present study, animals were divided into six groups (n = 6). The control group (group I) was injected with 0.25% of carboxymethyl cellulose. The arthritic control group (group II) was treated with Freund’s complete adjuvant (by injecting 0.1 mL). Prednisolone (10 mg/kg), a lower dose of MEAP (100 mg/kg), a medium dose of MEAP (200 mg/kg), and a higher dose of MEAP (400 mg/kg) were orally delivered to groups III, IV, V, and VI, respectively. Freund’s complete adjuvant was administered into the sub-plantar portion of the left-hind paw in all the groups except vehicle control to induce rheumatoid arthritis. Weight variation; joint diameter; paw volume; thermal and mechanical hyperalgesia; hematological, biochemical, and oxidative stress parameters; radiology; and a histopathological assessment of the synovial joint were observed in order to evaluate the antiarthritic effect of the methanolic extract of A. pallens. In this study, the estimated content of artemisinin was found to be 0.28% (per dry weight of the plant), which was in good agreement with the reported value. MEAP (200 and 400 mg/kg) caused a significant reduction in increased paw volume and joint diameter in arthritic rats while significantly increasing body weight and the mechanical threshold of thermal algesia. Moreover, complete blood counts and serum enzyme levels improved significantly. Radiological analysis showed a reduction in soft tissue swelling and small erosions. A histopathological examination of the cells revealed reduced cell infiltration and the erosion of joint cartilage in MEAP-administered arthritic rats. The present research suggests that the antiarthritic activity of the methanolic extract of A. pallens wall is promising, as evidenced by the findings explored in our rat model. Full article
(This article belongs to the Special Issue Treatment Strategies and Immune Responses in Rheumatic Diseases)
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Review

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18 pages, 622 KiB  
Review
Mitochondrial Dysfunction in Systemic Lupus Erythematosus: Insights and Therapeutic Potential
by Anastasia V. Poznyak, Nikolay A. Orekhov, Alexey V. Churov, Irina A. Starodubtseva, Dmitry F. Beloyartsev, Tatiana I. Kovyanova, Vasily N. Sukhorukov and Alexander N. Orekhov
Diseases 2024, 12(9), 226; https://doi.org/10.3390/diseases12090226 - 23 Sep 2024
Viewed by 1535
Abstract
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the presence of various serum autoantibodies and multi-system effects, predominantly affecting young female patients. The pathogenesis of SLE involves a combination of genetic factors, environmental triggers, and pathogen invasions that disrupt immune [...] Read more.
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the presence of various serum autoantibodies and multi-system effects, predominantly affecting young female patients. The pathogenesis of SLE involves a combination of genetic factors, environmental triggers, and pathogen invasions that disrupt immune cell activation, leading to the release of autoantibodies and chronic inflammation. Mitochondria, as the primary cellular powerhouses, play a crucial role in SLE development through their control of energy generation, reactive oxygen species (ROS) production, and cellular apoptotic pathways. Dysregulation of mitochondrial structure and function can contribute to the immune dysregulation, oxidative stress, and inflammation seen in SLE. Recent research has highlighted the impact of mitochondrial dysfunction on various immune cells involved in SLE pathogenesis, such as T-lymphocytes, B-lymphocytes, neutrophils, and plasmacytoid dendritic cells. Mitochondrial dysfunction in these immune cells leads to increased ROS production, disrupted mitophagy, and alterations in energy metabolism, contributing to immune dysregulation and inflammation. Moreover, genetic variations in mitochondrial DNA (mtDNA) and abnormalities in mitochondrial dynamics have been linked to the pathogenesis of SLE, exacerbating oxidative stress and immune abnormalities. Targeting mitochondrial function has emerged as a promising therapeutic approach for SLE. Drugs such as sirolimus, N-acetylcysteine, coenzyme Q10, and metformin have shown potential in restoring mitochondrial homeostasis, reducing oxidative stress, and modulating immune responses in SLE. These agents have demonstrated efficacy in preclinical models and clinical studies by improving disease activity, reducing autoantibody titers, and ameliorating organ damage in SLE patients. In conclusion, this review underscores the critical role of mitochondria in the pathogenesis of SLE and the potential of targeting mitochondrial dysfunction as a novel therapeutic strategy for improving outcomes in SLE patients. Further investigation into the mechanisms underlying mitochondrial involvement in SLE and the development of targeted mitochondrial therapies hold promise for advancing SLE treatment and enhancing patient care. Full article
(This article belongs to the Special Issue Treatment Strategies and Immune Responses in Rheumatic Diseases)
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Other

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11 pages, 456 KiB  
Brief Report
Serum 25-Hydroxyvitamin D Levels and Disease Activity in Patients with Systemic Lupus Erythematosus: An Exploratory Study in Western Mexico
by Daniela Deossa-Piedrahita, Berenice Vicente-Hernández, Sol Ramírez-Ochoa, Mauricio Alfredo Ambriz-Alarcón, Gabino Cervantes-Pérez, Gabino Cervantes-Guevara, Alejandro González-Ojeda, Clotilde Fuentes-Orozco, Francisco Javier Hernández-Mora, Luis Asdruval Zepeda-Gutiérrez, Jorge Isaac Michel-González, Janet Cristina Vázquez-Beltrán and Enrique Cervantes-Pérez
Diseases 2024, 12(12), 319; https://doi.org/10.3390/diseases12120319 - 8 Dec 2024
Viewed by 378
Abstract
Background and objectives: The correlation between diminished 25-hydroxyvitamin D (25-(OH)D) concentrations and heightened disease activity in systemic lupus erythematosus (SLE) patients remains contentious, as clinical studies have yielded conflicting outcomes—some propose a potential link, while others assert no relationship exists. Nonetheless, all studies [...] Read more.
Background and objectives: The correlation between diminished 25-hydroxyvitamin D (25-(OH)D) concentrations and heightened disease activity in systemic lupus erythematosus (SLE) patients remains contentious, as clinical studies have yielded conflicting outcomes—some propose a potential link, while others assert no relationship exists. Nonetheless, all studies report a significant prevalence of low 25-(OH)D levels among SLE patients. This study aimed to assess the frequency of low serum levels of 25-(OH)D in Mexican patients with SLE and to evaluate the correlation between 25-(OH)D deficiency or insufficiency and disease activity levels. Materials and Methods: This retrospective analysis comprised patients admitted to our hospital from November 2022 to October 2023, diagnosed with SLE, and had their serum 25-(OH)D levels tested upon admission. The frequency of low levels of 25-(OH)D was assessed, and clinical and demographic data were gathered to examine potential causes linked to 25-(OH)D deficiency or insufficiency. Results: A total of 61 patients were included, and 87% (n = 53) had low serum 25-(OH)D levels. Patients with 25-(OH)D deficiency (n = 21) were significantly younger (mean 23 vs. 39 years, p = 0.04) and had higher protein levels in 24 h urine protein (1.8 vs. 1.1 g/24 h, p = 0.006) than patients who presented only 25-(OH)D insufficiency, without significant differences in other indicators of disease activity. Conclusions: In this investigation, patients with SLE exhibited a high frequency of low serum levels of 25-(OH)D, consistent with existing literature; however, no significant correlations were identified between 25-(OH)D levels and indicators of disease activity. These findings require validation in subsequent research. Full article
(This article belongs to the Special Issue Treatment Strategies and Immune Responses in Rheumatic Diseases)
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