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Drug Therapy of Systemic Lupus Erythematosus

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 20 February 2026 | Viewed by 1019

Special Issue Editor


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Guest Editor
Department of Medicine, Karolinska Universitetssjukhuset, 17177 Stockholm, Sweden
Interests: systemic lupus erythematosus; autoimmunity

Special Issue Information

Dear Colleagues,

The landscape of SLE therapy has experienced significant progress following decades of setbacks and challenges, with the approvals of belimumab, anifrolumab, and voclosporin. More importantly, phase II trials have yielded promising results for TYK2 inhibitor deucravacitinib for general SLE and B-cell depletion therapy with obinutuzumab for lupus nephritis, potentially heralding successful phase III trials. Innovative cell therapies, particularly CD19 targeted CAR T-cell therapy, have demonstrated remarkable preliminary efficacy in SLE patients, paving the way for phase II/III trials. This evidence indicates a rapidly evolving field, with the potential to significantly alter SLE management and improve patient outcomes.

This Special Issue will comprehensively summarize the progress in SLE drug therapy over the past decade and explore emerging treatments. We seek submissions of original research, reviews, and clinical trial reports that delve into these advancements. To this end, contributions will highlight new pharmacological agents, cellular therapies, and personalized medicine approaches that are shaping the future of SLE treatment.

Dr. Dionysis Nikolopoulos
Guest Editor

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Keywords

  • systemic lupus erythematosus
  • treatment
  • drugs
  • tailored strategies
  • precision medicine
  • biologics
  • cell therapy
  • randomized clinical trials

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Published Papers (1 paper)

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Research

10 pages, 1604 KB  
Article
Anifrolumab Attenuates Follicular Helper T Cell Activation in Patients with Systemic Lupus Erythematosus
by Ádám Diós, Ágnes Gyetvai, Gábor Papp and Tünde Tarr
Int. J. Mol. Sci. 2025, 26(15), 7397; https://doi.org/10.3390/ijms26157397 - 31 Jul 2025
Viewed by 602
Abstract
Systemic lupus erythematosus (SLE) is a severe autoimmune disease characterized by autoantibody production and multi-organ involvement. Anifrolumab, a monoclonal antibody targeting the type I interferon (IFN) receptor, has been approved for the treatment of SLE. Our aim was to investigate the long-term effects [...] Read more.
Systemic lupus erythematosus (SLE) is a severe autoimmune disease characterized by autoantibody production and multi-organ involvement. Anifrolumab, a monoclonal antibody targeting the type I interferon (IFN) receptor, has been approved for the treatment of SLE. Our aim was to investigate the long-term effects of inhibited type I IFN signaling on circulating follicular helper T subsets (TFH), follicular regulatory T cells (TFR), and B lymphocyte subpopulations, reflecting the ongoing germinal center reactions in SLE patients. Peripheral blood samples were obtained from ten SLE patients before the initiation of anifrolumab treatment, and at months 6 and 12 of the intervention period. Flow cytometry analysis was performed to assess the frequencies of circulating TFH cell subsets, TFR cells, and certain B cell subpopulations. Serological parameters, including autoantibody levels and complement components, were determined as part of the routine diagnostic evaluation. We observed a significant and sustained reduction in the percentage of activated circulating TFH cells. Notably, the frequency of CXCR3CCR6+ TFH17 cells decreased, whereas the proportion of CXCR3+CCR6 TFH1 cells increased significantly. Furthermore, the proportion of the IgDCD27 double-negative B lymphocytes was also significantly reduced. These findings suggest that anifrolumab therapy attenuates TFH cell activation, which may contribute to its clinical efficacy by modulating germinal center responses in SLE. Full article
(This article belongs to the Special Issue Drug Therapy of Systemic Lupus Erythematosus)
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