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Cells
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The Molecular and Cellular Basis of Lupus 2021
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The Molecular and Cellular Basis of Lupus 2021

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 10032

Special Issue Editor

Dr. Anselm Mak

E-Mail Website
Guest Editor
Division of Rheumatology, Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore City, Singapore
Interests: systemic lupus erythematosus; inflammation; autoimmunity; T cells; neurocognition; functional MRI; meta-analyses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Systemic lupus erythematosus (SLE) is an autoimmune condition with a complicated pathophysiology that is not completely understood. While many molecular pathways and cellular alterations have been postulated and published in the literature, a number of clinical trials addressing these potentially pathological mechanisms have disappointingly failed to reach their respective primary endpoints, leading to the current paucity of targeted therapeutic agents that are capable of decelerating and even terminating the disease process and damage.
Nevertheless, some early and promising signals such as the success of the manipulation of the BAFF/ARPIL system, the antagonization of IL-12/23, and the use of IL-2 in the management of SLE are currently in the pipeline for further evaluation for the clinical management of SLE. Obviously, these potential successes will not materialize if the basic molecular and cellular mechanisms of these new targets that are involved in the pathophysiology of SLE are not fully explored, vigorously tested, and meticulously monitored.
This Special Issue of Cells aims to summarize the cutting-edge knowledge on the molecular and cellular basis of the pathogenesis and pathophysiology of SLE, in the hope of expanding the treatment armamentarium and, ultimately, personalized treatment for patients with SLE.

We are looking forward to your significant contributions.

Prof. Anselm Mak
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. 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

  • signaling pathways related to SLE
  • molecular alterations related to SLE
  • cell-surface, cytosolic, and nuclear–membrane receptors related to SLE
  • SLE-related cytokines and chemokines in SLE
  • Cell–cell interactions in SLE
  • mechanisms of organ involvement and damage in SLE

Published Papers (3 papers)

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Research

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11 pages, 796 KiB  
Article
Advanced Glycation End-Products (AGEs) and Their Soluble Receptor (sRAGE) in Women Suffering from Systemic Lupus Erythematosus (SLE)
by Agnieszka Nowak, Brygida Przywara-Chowaniec, Aleksandra Damasiewicz-Bodzek, Dominika Blachut, Ewa Nowalany-Kozielska and Krystyna Tyrpień-Golder
Cells 2021, 10(12), 3523; https://doi.org/10.3390/cells10123523 - 13 Dec 2021
Cited by 11 | Viewed by 2314
Abstract
Systemic lupus erythematosus (SLE) is characterized by abnormal action of the immune system and a state of chronic inflammation. The disease can cause life-threatening complications. Neoepitopes arising from interdependent glycation and oxidation processes might be an element of SLE pathology. The groups included [...] Read more.
Systemic lupus erythematosus (SLE) is characterized by abnormal action of the immune system and a state of chronic inflammation. The disease can cause life-threatening complications. Neoepitopes arising from interdependent glycation and oxidation processes might be an element of SLE pathology. The groups included in the study were 31 female SLE patients and 26 healthy female volunteers (the control group). Blood serum samples were obtained to evaluate concentrations of advanced glycation end-products (AGEs), carboxymethyllysine (CML), carboxyethyllysine (CEL), pentosidine, and a soluble form of the receptor for advanced glycation end-products (sRAGE). Compared to a healthy control group, the SLE patients exhibited a higher concentration of AGEs and a lower concentration of sRAGE in serum. There were no statistically significant differences in serum CML, CEL, and pentosidine concentrations between the groups. Therefore, SLE patients could be at risk of intensified glycation process and activation of the proinflammatory receptor for advanced glycation end-products (RAGE), which could potentially worsen the disease course; however, it is not clear which compounds contribute to the increased concentration of AGEs in the blood. Additionally, information about the cigarette smoking and alcohol consumption of the study participants was obtained. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis of Lupus 2021)
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15 pages, 1327 KiB  
Article
Elevated Interleukin-18 Receptor Accessory Protein Mediates Enhancement in Reactive Oxygen Species Production in Neutrophils of Systemic Lupus Erythematosus Patients
by Jie Ma, Ian Kar Yin Lam, Chak-Sing Lau and Vera Sau Fong Chan
Cells 2021, 10(5), 964; https://doi.org/10.3390/cells10050964 - 21 Apr 2021
Cited by 7 | Viewed by 3127
Abstract
Interleukin-18 receptor accessory protein (IL18RAP) is an indispensable subunit for the IL-18 receptor (IL-18R) complex’s ability to mediate high-affinity IL-18 binding and signalling transduction. Interest in IL-18 in systemic lupus erythematosus (SLE) has been mostly focused on its role as a type 1 [...] Read more.
Interleukin-18 receptor accessory protein (IL18RAP) is an indispensable subunit for the IL-18 receptor (IL-18R) complex’s ability to mediate high-affinity IL-18 binding and signalling transduction. Interest in IL-18 in systemic lupus erythematosus (SLE) has been mostly focused on its role as a type 1 T helper cell-driving cytokine. The functional significance of IL18RAP in mediating the IL-18-driven response in myeloid cells in SLE remains largely unexplored. This study aimed to investigate the expression and function significance of IL18RAP in neutrophils of SLE patients. By qRT-PCR and Western blot analyses, elevated expressions of IL18RAP mRNA and protein were observed in neutrophils from SLE patients—particularly those with a history of nephritis. IL18RAP expression correlated negatively with complement 3 level and positively with disease activity, with higher expression in patients exhibiting renal and immunological manifestations. The increased IL18RAP expression in SLE neutrophils could be attributed to elevated type I interferon level in sera. Functionally, neutrophils from SLE patients showed higher IL-18-mediated enhancement in reactive oxygen species (ROS) generation, which showed positive correlation with IL18RAP expression and could be neutralized by anti-IL18RAP blocking antibodies. Taken together, our findings suggest that IL-18 could contribute to SLE pathogenesis through mediation of neutrophil dysfunction via the upregulation of IL18RAP expression. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis of Lupus 2021)
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Review

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9 pages, 816 KiB  
Review
T Cells, Interleukin-2 and Systemic Lupus Erythematosus—From Pathophysiology to Therapy
by Anselm Mak
Cells 2022, 11(6), 980; https://doi.org/10.3390/cells11060980 - 12 Mar 2022
Cited by 3 | Viewed by 3853
Abstract
The phenotypic and functional complexities of T cells engender complicated and often confusing concepts as to how T cells ignite, accelerate and brake the inflammatory processes involved in systemic lupus erythematosus (SLE), let alone the plasticity of T cells that takes place under [...] Read more.
The phenotypic and functional complexities of T cells engender complicated and often confusing concepts as to how T cells ignite, accelerate and brake the inflammatory processes involved in systemic lupus erythematosus (SLE), let alone the plasticity of T cells that takes place under different immunological contexts. Nevertheless, being one of the prime survival factors of T cells, interleukin (IL)-2 plays a potentially critical role in many immunological scenarios during the pathophysiological process of SLE. Here, the pathophysiology of lupus T cells and current, as well as ongoing, therapeutic approaches of SLE that involve low-dose IL-2 administration will be highlighted. The mechanisms of IL-2 deficiency in SLE pathophysiology, the effects of low-dose IL-2 on T cells and restoration of lupus manifestations in murine SLE models, as well as the efficacy and safety of clinical trials that evaluated low-dose IL-2-containing regimens in patients with SLE will be discussed. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis of Lupus 2021)
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