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Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 9060

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Special Issue Editor

Prof. Dr. Chi Chiu Mok

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Guest Editor

Department of Medicine, Tuen Mun Hospital, New Territories, Hong Kong, China
Interests: systemic lupus erythematosus; particularly lupus nephritis; rheumatoid arthritis; glucocorticoid induced osteoporosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the availability of new immunomodulatory therapies, the survival of systemic lupus erythematosus (SLE) has failed to improve since the mid-1990s. Today, the need to develop novel management strategies for SLE that incorporate a better balance of efficacy and toxicity has yet to be met.

These strategies include the earlier recognition of major organ manifestations, such as lupus nephritis (LN), early aggressive therapies for high-risk patients to minimize organ damage, the better monitoring of disease activity, maintenance therapies to reduce disease flares, and the enhancement of medication adherence. The ultimate goal of SLE therapy is to induce and maintain a long-lasting remission, minimize organ damage and treatment-related complications, and to improve quality of life.

This Special Issue of “Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments“ in International Journal of Molecular Science (IJMS) covers works in different research areas of SLE. We welcome original articles, clinical trials, laboratory works, reviews, and meta-analyses.

Topics of interest include, but are not limited to, the following:

Genomic, transcriptomic, and metabolomic studies of systemic lupus erythematosus/ lupus nephritis (SLE/LN);
Classification criteria;
Disease activity indices;
Organ damage and comorbidities;
Serological, urine, and tissue biomarkers for the prediction of SLE/LN prognosis and flares;
Novel therapeutic modalities and strategies for SLE and LN.

Prof. Dr. Chi Chiu Mok
Guest Editor

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Keywords

lupus erythematosus
lupus nephritis
SLE
LN
organ damage
pathogenesis
biomarkers
genomic
transcriptomic
metabolomic
treatments
therapeutic

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Published Papers (6 papers)

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Research

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19 pages, 3453 KiB

Open AccessArticle

Defining Mechanistic Links Between the Non-Coding Variant rs17673553 in CLEC16A and Lupus Susceptibility

by Harikrishna Reddy Rallabandi, Manish Kumar Singh, Loren L. Looger and Swapan K. Nath

Int. J. Mol. Sci. 2025, 26(1), 314; https://doi.org/10.3390/ijms26010314 - 1 Jan 2025

Viewed by 1018

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by widespread inflammation and autoantibody production. Its development and progression involve genetic, epigenetic, and environmental factors. Although genome-wide association studies (GWAS) have repeatedly identified a susceptibility signal at 16p13, its fine-scale source and its functional and mechanistic role in SLE remain unclear. We used bioinformatics to prioritize likely functional variants and validated the top candidate through various experimental techniques, including clustered regularly interspaced short palindromic repeats (CRISPR)-based genome editing in B cells. To assess the functional impact of the proposed causal variant in C-type lectin domain family 16, member A (CLEC16A), we compared autophagy levels between wild-type (WT) and knock-out (KO) cells. Systematic bioinformatics analysis identified the highly conserved non-coding intronic variant rs17673553, with the risk allele apparently affecting enhancer function and regulating several target genes, including CLEC16A itself. Luciferase reporter assays followed by chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) validated this enhancer activity, demonstrating that the risk allele increases the binding of enhancer histone marks (H3K27ac and H3K4me1), the CTCF-binding factor, and key immune transcription factors (GATA3 and STAT3). Knock-down of GATA3 and STAT3 via siRNA led to a significant decrease in CLEC16A expression. These regulatory effects on the target gene were further confirmed using CRISPR-based genome editing and CRISPR-dCas9-based epigenetic activation/silencing. Functionally, WT cells exhibited higher levels of starvation-induced autophagy compared to KO cells, highlighting the role of CLEC16A and the rs17673553 locus in autophagy regulation. These findings suggest that the rs17673553 locus—particularly the risk allele—drives significant allele-specific chromatin modifications and binding of multiple transcription factors, thereby mechanistically regulating the expression of target autophagy-associated genes, including CLEC16A itself. This mechanism could potentially explain the association between rs17673553 and SLE, and could underlie the signal at 16p13. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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13 pages, 3170 KiB

Open AccessArticle

Neuropilin-1 as a Key Molecule for Renal Recovery in Lupus Nephritis: Insights from an NZB/W F1 Mouse Model

by Sebastian Sandoval, Cristina Solé, Blanca Joseph-Mullol, Maria Royo, Teresa Moliné, Alejandra Gabaldón and Josefina Cortés-Hernández

Int. J. Mol. Sci. 2024, 25(21), 11364; https://doi.org/10.3390/ijms252111364 - 22 Oct 2024

Cited by 1 | Viewed by 1085

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease affecting multiple organs, with lupus nephritis (LN) occurring in 40–50% of SLE patients. Despite advances in diagnosis and treatment, LN remains a major cause of morbidity and mortality, with 10–20% of patients progressing to end-stage renal disease (ESRD). While knowledge of LN’s pathogenesis has improved, mechanisms of renal recovery are still largely unexplored. Neuropilin-1 (NRP-1), a transmembrane receptor expressed in renal tissue, has emerged as a promising biomarker for assessing renal recovery in LN. This study evaluates and correlates longitudinal levels of NRP-1 with kidney histology using an NZB/W F1 mouse model of LN. A total of 30 mice were used, with 15 receiving intravenous cyclophosphamide (CYC) and 15 being untreated. NRP-1 levels were measured in urine and serum, and kidney samples were taken from a subgroup of mice for histological evaluation. The results demonstrated a progressive increase in renal and urinary NRP-1 expression, particularly notable at weeks 26 and 32. Urinary NRP-1 levels above 34.40 ng/mL were strong predictors of favorable renal response, showing 100% sensitivity and 88% specificity. These findings indicate a robust correlation between urinary NRP-1 levels and renal histological recovery, underscoring the potential of NRP-1 as a valuable biomarker for assessing renal response in LN. This study demonstrates that renal production of NRP-1 is linked to histological recovery and establishes a foundation for future research into the role of NRP-1 in lupus kidney recovery. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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Review

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19 pages, 1022 KiB

Open AccessReview

Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis

by Akshara Ramasamy and Chandra Mohan

Int. J. Mol. Sci. 2025, 26(6), 2621; https://doi.org/10.3390/ijms26062621 - 14 Mar 2025

Viewed by 459

Abstract

Lupus nephritis (LN), a significant complication of systemic lupus erythematosus (SLE), represents a challenging manifestation of the disease. One of the prominent pathophysiologic mechanisms targeting the renal parenchyma is fibrosis, a terminal process resulting in irreversible tissue damage that eventually leads to a decline in renal function and/or end-stage kidney disease (ESKD). Both glomerulosclerosis and interstitial fibrosis emerge as reliable prognostic indicators of renal outcomes. This article reviews the hallmarks of renal fibrosis in lupus nephritis, including the known and putative drivers of fibrogenesis. A better understanding of the cellular and molecular processes driving fibrosis in LN may help inform the development of therapeutic strategies for this disease, as well as the identification of individuals at higher risk of developing ESKD. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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23 pages, 2898 KiB

Open AccessReview

A Comprehensive Review of Fc Gamma Receptors and Their Role in Systemic Lupus Erythematosus

by Jesús Sepúlveda-Delgado, Luis Llorente and Susana Hernández-Doño

Int. J. Mol. Sci. 2025, 26(5), 1851; https://doi.org/10.3390/ijms26051851 - 21 Feb 2025

Cited by 1 | Viewed by 937

Abstract

Receptors for the immunoglobulin G constant fraction (FcγRs) are widely expressed in cells of the immune system. Complement-independent phagocytosis prompted FcγR research to show that the engagement of IgG immune complexes with FcγRs triggers a variety of cell host immune responses, such as phagocytosis, antibody-dependent cell cytotoxicity, and NETosis, among others. However, variants of these receptors have been implicated in the development of and susceptibility to autoimmune diseases such as systemic lupus erythematosus. Currently, the knowledge of FcγR variants is a required field of antibody therapeutics, which includes the engineering of recombinant soluble human Fc gamma receptors, enhancing the inhibitory and blocking the activating FcγRs function, vaccines, and organ transplantation. Importantly, recent interest in FcγRs is the antibody-dependent enhancement (ADE), a mechanism by which the pathogenesis of certain viral infections is enhanced. ADEs may be responsible for the severity of the SARS-CoV-2 infection. Therefore, FcγRs have become a current research topic. Therefore, this review briefly describes some of the historical knowledge about the FcγR type I family in humans, including the structure, affinity, and mechanism of ligand binding, FcγRs in diseases such as systemic lupus erythematosus (SLE), and the potential therapeutic approaches related to these receptors in SLE. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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20 pages, 622 KiB

Open AccessReview

Advances in Targeted Therapy for Systemic Lupus Erythematosus: Current Treatments and Novel Approaches

by Kazusa Saegusa, Yumi Tsuchida, Toshihiko Komai, Haruka Tsuchiya and Keishi Fujio

Int. J. Mol. Sci. 2025, 26(3), 929; https://doi.org/10.3390/ijms26030929 - 23 Jan 2025

Cited by 1 | Viewed by 3621

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse clinical manifestations that can lead to severe organ damage. The complex pathophysiology of SLE makes treatment selection difficult. This review examines the current evidence for biological therapies in SLE, including the anti-B cell activating factor antibody belimumab; the type I interferon receptor antagonist anifrolumab; the novel calcineurin inhibitor voclosporin; and rituximab, which targets CD20 on B cells. We also describe emerging therapies, including novel agents in development and CD19-directed chimeric antigen receptor (CAR) T cell therapy, which has shown promise in early clinical experience. Recent advances in biomarker research, including interferon signatures and transcriptomic profiles, may facilitate patient stratification and treatment selection. This review offers insights into current and future treatment strategies for patients with SLE by analyzing clinical trial results and recent immunological findings. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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12 pages, 622 KiB

Open AccessReview

The Potential Use of Arsenic Trioxide in the Treatment of Systemic Lupus Erythematosus

by Tsz Ching Mok and Chi Chiu Mok

Int. J. Mol. Sci. 2024, 25(17), 9577; https://doi.org/10.3390/ijms25179577 - 4 Sep 2024

Cited by 1 | Viewed by 1642

Abstract

Arsenic trioxide (ATO) is now part of the standard regimen for the treatment of newly diagnosed and relapsed acute promyelocytic leukemia. The availability of an oral form of ATO has greatly reduced the incidence of cardiotoxicity as compared to intravenous (IV) administration. Increasing evidence suggests that ATO has anti-inflammatory properties that may be useful for the treatment of autoimmune diseases. These include the modulation of Treg cell activation, Th1/Th2 and Th17/Treg balance, depletion of activated T cells and plasmacytoid dendritic cells, and influence of B-cell differentiation, leading to reduced autoantibody and cytokine production. ATO has also been shown to induce apoptosis of activated fibroblast-like synoviocytes through the generation of reactive oxygen species and alter the gut microbiota in collagen-induced arthritis. Despite the emergence of newer treatment modalities, the treatment of systemic lupus erythematosus (SLE), especially refractory manifestations, remains a challenge, owing to the paucity of effective biological and targeted therapies that are devoid of adverse effects. Oral ATO is an attractive option for the treatment of SLE because of the lower cost of production, convenience of administration, and reduced cardiotoxicity. This article summarizes the anti-inflammatory mechanisms of ATO and its potential application in the treatment of SLE and other rheumatic diseases. Full article

(This article belongs to the Special Issue Advances in Lupus Erythematosus and Lupus Nephritis: Pathogenesis, Biomarkers and Treatments)

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