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Immunopathogenesis and Novel Therapeutics Strategies of Systemic Lupus Erythematosus 2.0
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Immunopathogenesis and Novel Therapeutics Strategies of Systemic Lupus Erythematosus 2.0

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: 30 June 2024 | Viewed by 3282

Special Issue Editors

Prof. Dr. Marzena Olesińska

E-Mail Website
Guest Editor
Department of Connective Tissue Diseases, National Institute of Geriatrics, Rheumatology and Rehabilitation, 02-637 Warsaw, Poland
Interests: rheumatology; internal diseases; systemic lupus erythematosus; arthritis; systemic sclerosis; dermatomyositis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Przemysław Kotyla

E-Mail Website
Guest Editor
Department of Internal Medicine, Rheumatology and Clinical Immunology, Faculty in Katowice, Medical University of Silesia, Katowice, Poland
Interests: systemic lupus erythematosus; rheumatic diseases; autoimmunity; clinical rheumatology; autoimmune disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Systemic lupus erythematosus (SLE) is a connective tissue disease that may serve as a prototype for almost all autoimmune diseases. Its diversity of clinical presentations and involvement in all vitally important internal organs is challenging for treating physicians. Moreover, despite the enormous progress in rheumatology and clinical immunology, the pathophysiological background of the disease is still not understood completely. From a clinical point of view, corticosteroids and immunosuppressants are still the gold standard for the treatment of SLE. The main reason for this is still the lack of new treatment strategies that are safe and efficacious for SLE. Therefore, understanding the SLE pathogenic background and disease-driving mechanisms will contribute to the development of novel therapeutic strategies.

SLE pathogenesis is complex and, obviously, none of the single pathological mechanisms might be responsible for all SLE presentations. Moreover, the existence of many pathological theories suggests quite convincingly that none of them are universal or explain the disease satisfactorily. In the course of SLE, several immunological phenomena may be observed, such as the loss of tolerance to self-antigens, autoreactive T- and B-cell activation, the synthesis of autoantibodies, and the activation of interferon. In recent years, advances in immunology have translated to the identification of several molecular and cellular targets, the modulation of which may exert therapeutic potential in the disease.

This Special Issue is designed as a platform to provide recent research advantages that focus on understanding the immuno-pathological mechanisms, biomarkers, and novel therapeutic strategies in SLE. Both review and research papers are welcomed. Please note that pure clinical or model studies are unsuitable for this journal, but clinical submissions with biomolecular studies are welcome. Topics include, but are not limited to, the following:

  • The genetic background of SLE;
  • The epigenetic regulation of lupus;
  • Cellular and molecular mechanisms in lupus;
  • The role of cytokine networks in lupus progression;
  • Innate and adaptive immunity in SLE;
  • The role of immunocompetent cells in lupus pathogenesis and disease mechanisms;
  • The role of interferon and interferon signature in lupus pathogenesis;
  • Novel lupus biomarkers in SLE diagnosis and monitoring disease activity;
  • Novel therapeutics and new treatment strategies for lupus.

Prof. Dr. Marzena Olesińska
Prof. Dr. Przemysław Kotyla
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 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. 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

  • systemic lupus erythematosus
  • SLE pathogenesis
  • the epigenetic regulation of lupus
  • the genetic background of SLE
  • interferon
  • cytokine networks
  • innate immunity
  • adaptive immunity

Published Papers (3 papers)

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Research

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19 pages, 5086 KiB  
Article
Precise Targeting of Autoantigen-Specific B Cells in Lupus Nephritis with Chimeric Autoantibody Receptor T Cells
by Cristina Solé, Maria Royo, Sebastian Sandoval, Teresa Moliné, Alejandra Gabaldón and Josefina Cortés-Hernández
Int. J. Mol. Sci. 2024, 25(8), 4226; https://doi.org/10.3390/ijms25084226 - 11 Apr 2024
Viewed by 442
Abstract
Despite conventional therapy, lupus nephritis (LN) remains a significant contributor to short- and long-term morbidity and mortality. B cell abnormalities and the production of autoantibodies against nuclear complexes like anti-dsDNA are recognised as key players in the pathogenesis of LN. To address the [...] Read more.
Despite conventional therapy, lupus nephritis (LN) remains a significant contributor to short- and long-term morbidity and mortality. B cell abnormalities and the production of autoantibodies against nuclear complexes like anti-dsDNA are recognised as key players in the pathogenesis of LN. To address the challenges of chronic immunosuppression associated with current therapies, we have engineered T cells to express chimeric autoantibody receptors (DNA-CAART) for the precise targeting of B cells expressing anti-dsDNA autoantibodies. T cells from LN patients were transduced using six different CAAR vectors based on their antigen specificity, including alpha-actinin, histone-1, heparan sulphate, or C1q. The cytotoxicity, cytokine production, and cell–cell contact of DNA-CAART were thoroughly investigated in co-culture experiments with B cells isolated from patients, both with and without anti-dsDNA positivity. The therapeutic effects were further evaluated using an in vitro immune kidney LN organoid. Among the six proposed DNA-CAART, DNA4 and DNA6 demonstrated superior selectively cytotoxic activity against anti-dsDNA+ B cells. Notably, DNA4-CAART exhibited improvements in organoid morphology, apoptosis, and the inflammatory process in the presence of IFNα-stimulated anti-dsDNA+ B cells. Based on these findings, DNA4-CAART emerge as promising candidates for modulating autoimmunity and represent a novel approach for the treatment of LN. Full article
(This article belongs to the Special Issue Immunopathogenesis and Novel Therapeutics Strategies of Systemic Lupus Erythematosus 2.0)
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Review

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22 pages, 943 KiB  
Review
Emerging Molecular and Synaptic Targets for the Management of Chronic Pain Caused by Systemic Lupus Erythematosus
by Han-Rong Weng
Int. J. Mol. Sci. 2024, 25(7), 3602; https://doi.org/10.3390/ijms25073602 - 22 Mar 2024
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Abstract
Patients with systemic lupus erythematosus (SLE) frequently experience chronic pain due to the limited effectiveness and safety profiles of current analgesics. Understanding the molecular and synaptic mechanisms underlying abnormal neuronal activation along the pain signaling pathway is essential for developing new analgesics to [...] Read more.
Patients with systemic lupus erythematosus (SLE) frequently experience chronic pain due to the limited effectiveness and safety profiles of current analgesics. Understanding the molecular and synaptic mechanisms underlying abnormal neuronal activation along the pain signaling pathway is essential for developing new analgesics to address SLE-induced chronic pain. Recent studies, including those conducted by our team and others using the SLE animal model (MRL/lpr lupus-prone mice), have unveiled heightened excitability in nociceptive primary sensory neurons within the dorsal root ganglia and increased glutamatergic synaptic activity in spinal dorsal horn neurons, contributing to the development of chronic pain in mice with SLE. Nociceptive primary sensory neurons in lupus animals exhibit elevated resting membrane potentials, and reduced thresholds and rheobases of action potentials. These changes coincide with the elevated production of TNFα and IL-1β, as well as increased ERK activity in the dorsal root ganglion, coupled with decreased AMPK activity in the same region. Dysregulated AMPK activity is linked to heightened excitability in nociceptive sensory neurons in lupus animals. Additionally, the increased glutamatergic synaptic activity in the spinal dorsal horn in lupus mice with chronic pain is characterized by enhanced presynaptic glutamate release and postsynaptic AMPA receptor activation, alongside the reduced activity of glial glutamate transporters. These alterations are caused by the elevated activities of IL-1β, IL-18, CSF-1, and thrombin, and reduced AMPK activities in the dorsal horn. Furthermore, the pharmacological activation of spinal GPR109A receptors in microglia in lupus mice suppresses chronic pain by inhibiting p38 MAPK activity and the production of both IL-1β and IL-18, as well as reducing glutamatergic synaptic activity in the spinal dorsal horn. These findings collectively unveil crucial signaling molecular and synaptic targets for modulating abnormal neuronal activation in both the periphery and spinal dorsal horn, offering insights into the development of analgesics for managing SLE-induced chronic pain. Full article
(This article belongs to the Special Issue Immunopathogenesis and Novel Therapeutics Strategies of Systemic Lupus Erythematosus 2.0)
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25 pages, 1595 KiB  
Review
Potential Therapeutic Application and Mechanism of Action of Stem Cell-Derived Extracellular Vesicles (EVs) in Systemic Lupus Erythematosus (SLE)
by Sushmitha Rajeev Kumar, Rajalingham Sakthiswary and Yogeswaran Lokanathan
Int. J. Mol. Sci. 2024, 25(4), 2444; https://doi.org/10.3390/ijms25042444 - 19 Feb 2024
Viewed by 1537
Abstract
Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease that affects nearly 3.41 million people globally, with 90% of the cases affecting women of childbearing age. SLE is a complex disease due to the interplay of various immunological pathways and mechanisms. This scoping [...] Read more.
Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease that affects nearly 3.41 million people globally, with 90% of the cases affecting women of childbearing age. SLE is a complex disease due to the interplay of various immunological pathways and mechanisms. This scoping review aims to highlight the latest research findings on the therapeutic mechanisms of action of EVs in SLE. Relevant research articles were identified using the PRISMA framework from databases such as PubMed/MEDLINE (National Library of Medicine), Scopus (Elsevier), and Web of Science: Core Collection (Clarivate Analytics) from July 2023 to October 2023. Eleven studies met the inclusion criteria and thus were included in this scoping review. The findings showed that EVs have therapeutic effects on ameliorating the disease progression of SLE. EVs can reduce the pro-inflammatory cytokines and increase the anti-inflammatory cytokines. Moreover, EVs can increase the levels of regulatory T cells, thus reducing inflammation. EVs also have the potential to regulate B cells to alleviate SLE and reduce its adverse effects. The scoping review has successfully analysed the therapeutic potential in ameliorating the disease progression of SLE. The review also includes prospects to improve the effects of EVs further to increase the therapeutic effects on SLE. Full article
(This article belongs to the Special Issue Immunopathogenesis and Novel Therapeutics Strategies of Systemic Lupus Erythematosus 2.0)
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