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Cells
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Systemic Lupus Erythematosus: Update of Pathogenesis and Target Therapy
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Systemic Lupus Erythematosus: Update of Pathogenesis and Target Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 5632

Special Issue Editors

Prof. Dr. Ji-Yih Chen

E-Mail Website
Guest Editor
Department of Medicine, Division of Allergy, Immunology and Rheumatology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan 33302, Taiwan
Interests: systemic lupus erythematosus; AS and RA functional genomic characterization, gene signature and immune cells development
Dr. I-Tsu Chyuan

E-Mail Website
Guest Editor
Department of Internal Medicine, Cathay General Hospital, Taipei 10630, Taiwan
Interests: systemic lupus erythematosus; immunology

Special Issue Information

Dear Colleagues,

SLE is a challenging disease with complicated pathophysiology including genetic, epigenetic, and environmental exposures that promote loss of tolerance and systemic autoimmunity, resulting in organ damage. Several important new studies try to pinpoint the critical pathways that contribute to SLE's wide clinical range. Achieving and maintaining illness remission, as well as long-term patient survival, are the optimal therapy goals. However, in terms of safety and efficacy, the most recently approved immune target biologic medicines did not surpass standard immunosuppressive therapy.

The method for forecasting SLE activity has the added benefit of allowing for better disease monitoring and evaluation of treatment approaches. Emerging omics applications of genomic, transcriptome, proteomic, microbiome, and metabolomic analysis have revealed distinct functional genomic risk variants, gene signature stratifications, disease-associated metabolites or proteins, and microbiome profiling, revealing new immune-regulatory pathways and further predicting lupus disease heterogeneity and activity.

Dissecting the molecular abnormalities of dysregulated signaling events and immune cells' pathogenetic faults will lead to the discovery of new predictive biomarkers and therapeutic targets.

The goals of this Special Issue are to bring together fresh research and extensive reviews to better understand the SLE heterogeneous disease entity, genetic population differences, prospective cellular targets and signaling components, and lastly, to achieve therapeutic success with SLE.

Prof. Dr. Ji-Yih Chen
Dr. I-Tsu Chyuan
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. Cells 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 2700 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

  • functional genome
  • transcriptome signature
  • single cell RNAseq
  • epigenetic
  • microbiome
  • signaling pathways
  • immunometabolism
  • proteomic and metabolomic
  • biomarker
  • target therapy

Published Papers (3 papers)

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Research

16 pages, 2079 KiB  
Article
Comprehensive Co-Inhibitory Receptor (Co-IR) Expression on T Cells and Soluble Proteins in Rheumatoid Arthritis
by Chin-Man Wang, Yeong-Jian Jan Wu, Li-Yu Huang, Jian-Wen Zheng and Ji-Yih Chen
Cells 2024, 13(5), 403; https://doi.org/10.3390/cells13050403 - 26 Feb 2024
Viewed by 1000
Abstract
Co-inhibitory receptors (Co-IRs) are essential in controlling the progression of immunopathology in rheumatoid arthritis (RA) by limiting T cell activation. The objective of this investigation was to determine the phenotypic expression of Co-IR T cells and to assess the levels of serum soluble [...] Read more.
Co-inhibitory receptors (Co-IRs) are essential in controlling the progression of immunopathology in rheumatoid arthritis (RA) by limiting T cell activation. The objective of this investigation was to determine the phenotypic expression of Co-IR T cells and to assess the levels of serum soluble PD-1, PDL-2, and TIM3 in Taiwanese RA patients. Methods: Co-IRs T cells were immunophenotyped employing multicolor flow cytometry, and ELISA was utilized for measuring soluble PD-1, PDL-2, and TIM3. Correlations have been detected across the percentage of T cells expressing Co-IRs (MFI) and different indicators in the blood, including ESR, high-sensitivity CRP (hsCRP), 28 joint disease activity scores (DAS28), and soluble PD-1/PDL-2/TIM3. Results: In RA patients, we recognized elevated levels of PD-1 (CD279), CTLA-4, and TIGIT in CD4+ T cells; TIGIT, HLA-DR, TIM3, and LAG3 in CD8+ T cells; and CD8+CD279+TIM3+, CD8+HLA-DR+CD38+ T cells. The following tests were revealed to be correlated with hsCRP: CD4/CD279 MFI, CD4/CD279%, CD4/TIM3%, CD8/TIM3%, CD8/TIM3 MFI, CD8/LAG3%, and CD8+HLA-DR+CD38+%. CD8/LAG3 and CD8/TIM3 MFIs are linked to ESR. DAS28-ESR and DAS28-CRP exhibited relationships with CD4/CD127 MFI, CD8/CD279%, and CD8/CD127 MFI, respectively. CD4+CD279+TIM3+% was correlated with DAS28-ESR (p = 0.0084, N = 46), DAS28-CRP (p = 0.007, N = 47), and hsCRP (p = 0.002, N = 56), respectively. In the serum of patients with RA, levels of soluble PD-1, PDL-2, and Tim3 were extremely elevated. CD4+ TIM3+% (p = 0.0089, N = 46) and CD8+ TIM3+% (p = 0.0305, N = 46) were correlated with sTIM3 levels; sPD1 levels were correlated with CD4+CD279+% (p < 0.0001, N = 31) and CD3+CD279+% (p = 0.0084, N = 30). Conclusions: Co-IR expressions on CD4+ and CD8+ T cells, as well as soluble PD-1, PDL-2, and TIM3 levels, could function as indicators of disease activity and potentially play crucial roles in the pathogenesis of RA. Full article
(This article belongs to the Special Issue Systemic Lupus Erythematosus: Update of Pathogenesis and Target Therapy)
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17 pages, 4289 KiB  
Article
Systemic Lupus Erythematosus Patients with DNASE1L3·Deficiency Have a Distinctive and Specific Genic Circular DNA Profile in Plasma
by Daniela Gerovska and Marcos J. Araúzo-Bravo
Cells 2023, 12(7), 1061; https://doi.org/10.3390/cells12071061 - 31 Mar 2023
Cited by 4 | Viewed by 2134
Abstract
Cell-free (cf) extrachromosomal circular DNA (eccDNA) has a potential clinical application as a biomarker. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a complex immunological pathogenesis, associated with autoantibody synthesis. A previous study found that SLE patients with deoxyribonuclease 1-like 3 [...] Read more.
Cell-free (cf) extrachromosomal circular DNA (eccDNA) has a potential clinical application as a biomarker. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a complex immunological pathogenesis, associated with autoantibody synthesis. A previous study found that SLE patients with deoxyribonuclease 1-like 3 (DNASE1L3) deficiency exhibit changes in the frequency of short and long eccDNA in plasma compared to controls. Here, using the DifCir method for differential analysis of short-read sequenced purified eccDNA data based on the split-read signal of the eccDNA on circulomics data, we show that SLE patients with DNASE1L3 deficiency have a distinctive profile of eccDNA excised by gene regions compared to controls. Moreover, this profile is specific; cf-eccDNA from the top 93 genes is detected in all SLE with DNASE1L3 deficiency samples, and none in the control plasma. The top protein coding gene producing eccDNA-carrying gene fragments is the transcription factor BARX2, which is involved in skeletal muscle morphogenesis and connective tissue development. The top gene ontology terms are ‘positive regulation of torc1 signaling’ and ‘chondrocyte development’. The top Harmonizome terms are ‘lymphopenia’, ‘metabolic syndrome x’, ‘asthma’, ‘cardiovascular system disease‘, ‘leukemia’, and ‘immune system disease’. Here, we show that gene associations of cf-eccDNA can serve as a biomarker in the autoimmune rheumatic diseases. Full article
(This article belongs to the Special Issue Systemic Lupus Erythematosus: Update of Pathogenesis and Target Therapy)
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10 pages, 2528 KiB  
Article
UC-BSCs Exosomes Regulate Th17/Treg Balance in Patients with Systemic Lupus Erythematosus via miR-19b/KLF13
by Jianxin Tu, Nan Zheng, Chentong Mao, Shan Liu, Hongxing Zhang and Li Sun
Cells 2022, 11(24), 4123; https://doi.org/10.3390/cells11244123 - 19 Dec 2022
Cited by 10 | Viewed by 2010
Abstract
Umbilical cord blood mesenchymal stem cells (UC-BSCs) are cells with low immunogenicity and differentiation potential, and the transfer of exosomes carried by UC-BSCs can regulate innate and adaptive immunity and affect immune homeostasis. This is an area of focus for autoimmune illnesses such [...] Read more.
Umbilical cord blood mesenchymal stem cells (UC-BSCs) are cells with low immunogenicity and differentiation potential, and the transfer of exosomes carried by UC-BSCs can regulate innate and adaptive immunity and affect immune homeostasis. This is an area of focus for autoimmune illnesses such as systemic lupus erythematosus (SLE). The target of this research was to investigate the immunomodulatory effect of exosomes produced from mesenchymal stem cells on SLE and its mechanism. After isolation of peripheral blood mononuclear cells (PBMC) from the SLE group and healthy group and treatment of SLE-derived PBMCs with UC-BSC-derived exosomes, the mRNA levels of corresponding factors in cells under different treatments were determined by RT-PCR, Th17/Treg content was analyzed by FCM (flow cytometry), and the targeted binding of microRNA-19b (miR-19b) to KLF13 was identified by in vitro experiments and bioinformatics analysis. The findings demonstrated that PBMC cells from SLE patients had higher proportions of Th17 subsets than the control group, whereas Treg subgroups with lower percentages were discovered. miR-19b’s expression level was markedly reduced, which was inversely associated to the concentration of KLF13. In vitro experiments show that UC-BSC-derived exosome treatment can target KLF13 expression by increasing the miR-19b level, thereby regulating Th17/Treg balance and inhibiting the expression of inflammatory factors. According to the study’s findings, SLE patients have dysregulated expression of the genes miR-19b and KLF13, and UC-BSC exosomes could regulate Th17/Treg cell balance and inflammatory factor expression in SLE patients through miR-19b/KLF13. Full article
(This article belongs to the Special Issue Systemic Lupus Erythematosus: Update of Pathogenesis and Target Therapy)
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