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Systemic Lupus Erythematosus: Current Trends and Therapeutic Innovations
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Systemic Lupus Erythematosus: Current Trends and Therapeutic Innovations

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 28 August 2025 | Viewed by 152

Special Issue Editor

Dr. Giuseppe Barilaro

E-Mail Website
Guest Editor
Department of Internal Medicine, Sant'Eugenio Hospital, Rome, Italy
Interests: systemic lupus erythematosus; rheumatic diseases; antiphospholipid syndrome; immune-mediated disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect any organ in the body, with the skin, joints, blood cells, kidney, lungs, heart, and central nervous system being more frequently involved. As with other autoimmune diseases, the pathogenesis of SLE relies on an anomaly in the immune system, where it is not capable of recognizing the body’s own antigens and attacks a patient’s cells.

SLE diagnosis is based on an array of clinical symptoms (e.g., arthralgia, shortness of breath, and tiredness) and signs (e.g., fever, joint edema and inflammation, and pleural effusion), and laboratory tests (blood count, renal function parameters, and proteinuria), along with non-specific and specific auto-antibodies, radiological tests, and histological exams (especially for kidney involvement). Meanwhile, other diseases should be ruled out. Diagnosis is not always straightforward, due to the diversity of clinical manifestations, which not always appear in the same way and at the same time, and sometimes it is possible after many years of follow-up.

The JCM is pleased to announce a Special Issue called “Systemic Lupus Erythematosus: Current Trends and Therapeutic Innovations”, which aims to provide an overview of current and new knowledge on the clinical features, diagnostic tools, treatment strategies (with a particular focus on new targeted therapies), biomarkers, and long-term outcomes of SLE.

Dr. Giuseppe Barilaro
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. Journal of Clinical Medicine 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 2600 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

  • systemic lupus erythematosus
  • autoantibodies
  • biomarkers
  • therapeutic drugs
  • lupus nephritis
  • quality of life
  • new treatment strategies

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Published Papers (1 paper)

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Research

13 pages, 2623 KiB  
Article
Association of TNF-alpha Promoter Polymorphisms with Disease Susceptibility, mRNA Expression, and Lupus Nephritis in Mexican Patients with Systemic Lupus Erythematosus
by Diana Celeste Salazar-Camarena, Claudia Azucena Palafox-Sánchez, Noemí Espinoza-García, Jorge Armando Guareña-Casillas, María Paulina Reyes-Mata, Jhonatan Velador-Mendoza and Miguel Marín-Rosales
J. Clin. Med. 2025, 14(11), 3693; https://doi.org/10.3390/jcm14113693 (registering DOI) - 25 May 2025
Abstract
Background/Objectives: A case-control study was conducted to determine the association of the −238 G>A and −308 G>A TNF-alpha (TNFA) promoter polymorphisms with mRNA and protein expression in 180 Systemic Lupus Erythematosus (SLE) patients and 186 control subjects (CS) from western [...] Read more.
Background/Objectives: A case-control study was conducted to determine the association of the −238 G>A and −308 G>A TNF-alpha (TNFA) promoter polymorphisms with mRNA and protein expression in 180 Systemic Lupus Erythematosus (SLE) patients and 186 control subjects (CS) from western Mexico. Methods: Genotyping was performed using the PCR-RFLP method. TNFA mRNA expression was assessed by real-time quantitative PCR, and soluble TNF-α (sTNF-α) levels were quantified by ELISA. For comparison groups, Chi-square, Mann–Whitney U, or Kruskal–Wallis tests were used. Spearman’s rank correlation coefficient determined the correlation between variables. The Area Under the Curve was used to determine the diagnosing performance of sTNF-α. Results: No differences were found in the genotype distribution of −238 G>A and −308 G>A TNFA polymorphisms between SLE patients and CS. However, the −238A allele was associated with increased SLE susceptibility (OR 1.18 CI 95% 1.02–3.50, p = 0.037). Also, logistic regression analysis showed that LN risk was significantly higher in carriers of the −308A allele (OR 3.11 IC95% 1.15–6.43; p = 0.002). On the other hand, the TNFA mRNA expression was 3.3-fold higher in SLE compared to CS. SLE patients with −308 GG genotype showed higher TNFA mRNA expression compared to GA+AA genotype carriers (p < 0.01). Regarding sTNFa levels, SLE patients showed higher concentration than CS, mainly in lupus nephritis (LN), with a weak negative correlation with estimated Glomerular Filtration Rate and an acceptable accuracy for diagnosing SLE and LN, with areas under the curve of 0.61 and 0.65, respectively. Conclusions: The −238 A allele and −308 A allele of the TNFA gene are linked to a higher risk of susceptibility to SLE and LN in the western Mexican population. Additionally, SLE patients exhibited increased TNF-alpha gene expression and sTNF-α, particularly in LN, demonstrating acceptable diagnostic performance. Full article
(This article belongs to the Special Issue Systemic Lupus Erythematosus: Current Trends and Therapeutic Innovations)
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