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Cells
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Molecular Insights into Systemic Lupus Erythematosus Pathogenesis: From Genes to...
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Molecular Insights into Systemic Lupus Erythematosus Pathogenesis: From Genes to Immune Signaling

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

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 1615

Special Issue Editor

Dr. Shunichi Shiozawa

E-Mail Website
Guest Editor
Institute for Rheumatic Diseases, Ashiya, Japan
Interests: systemic lupus erythematosus; pathogenesis; cause of autoimmunity

Special Issue Information

Dear Colleagues,

I am a professor of medicine whose work contributes significantly to the clarification of the pathogenesis of systemic lupus erythematosus and autoimmune diseases.

As an invited editor, I hereby invite review manuscripts on the pathogenesis of SLE, the review based on author’s direct evidence. Review articles expounding the author’s direct evidence are highly useful for and influential in scientific community because of the prohibition of critical discussions in many recent scientific journals. There is extensive indirect evidence of the pathogenesis of SLE. However, this contributes nothing to the clarification of the pathogenesis of SLE and to the progress of science and medicine. I encourage authors with direct evidence on the pathogenesis of SLE to post their review manuscripts.

Dr. Shunichi Shiozawa
Guest Editor

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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.

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Keywords

  • SLE
  • pathogenesis
  • cause
  • infectious
  • TCR revision

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Published Papers (2 papers)

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Research

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18 pages, 7709 KiB  
Article
Increased Sensitivity to Ionizing Radiation in a Relevant Subset of Patients with Cancer and Systemic Lupus Erythematosus
by Hannah Schenker, Lukas Kuhlmann, Dorothee Kaudewitz, Barbara Schuster, Sabine Semrau, Charlotte Schmitter, Raphaela Voigt, Ricarda Merten, Hans Geinitz, Rainer Fietkau, Sebastian Böltz, Georg Schett and Luitpold V. Distel
Cells 2025, 14(8), 569; https://doi.org/10.3390/cells14080569 - 9 Apr 2025
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Abstract
It has long been hypothesized that systemic lupus erythematosus (SLE) increases radiosensitivity, but recent studies have yielded mixed results. We studied individual radiosensitivity in 70 individuals with SLE using chromosomal aberrations as biomarkers of radiosensitivity. In total, 33 patients with SLE and 37 [...] Read more.
It has long been hypothesized that systemic lupus erythematosus (SLE) increases radiosensitivity, but recent studies have yielded mixed results. We studied individual radiosensitivity in 70 individuals with SLE using chromosomal aberrations as biomarkers of radiosensitivity. In total, 33 patients with SLE and 37 patients with SLE and additional oncologic diseases were compared with healthy individuals and with patients with rectal and breast cancer. Individual radiosensitivity was assessed by ex vivo irradiation of G0 blood lymphocytes followed by three-color fluorescence in situ hybridization of chromosomes 1, 2, and 4. SLE patients have slightly higher background rates of chromosomal aberrations than healthy individuals and lower rates than cancer patients. Non-oncologic SLE patients show a rate of chromosomal aberrations similar to that seen in healthy individuals. The outliers in this group, who clearly show increased radiosensitivity, fall between healthy individuals and cancer patients. Patients with SLE and cancer have significantly higher chromosome aberration rates compared to healthy individuals (p < 0.001) and patients with isolated cancer (p = 0.007) or isolated SLE (p = 0.004). The proportion of radiosensitive patients in the oncologic SLE cohort is high, with 45% of patients showing increased radiosensitivity. There is a weak association between anti-Ro-52 autoantibodies and radiosensitivity. Based on the radiosensitivity measurement, radiation dose reduction was recommended in 11 oncological SLE patients and was successfully achieved in 5 patients by up to 21% of the dose per fraction. In the oncologic SLE cohort, a substantial portion of individuals show increased radiosensitivity. Full article
(This article belongs to the Special Issue Molecular Insights into Systemic Lupus Erythematosus Pathogenesis: From Genes to Immune Signaling)
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Review

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17 pages, 1438 KiB  
Review
Pathogenesis of Autoimmunity/Systemic Lupus Erythematosus (SLE)
by Shunichi Shiozawa
Cells 2025, 14(14), 1080; https://doi.org/10.3390/cells14141080 - 15 Jul 2025
Viewed by 533
Abstract
SLE is characterized by the generation of a variety of autoantibodies including anti-dsDNA autoantibodies, causing damage in various organs. If autoimmunity is defined by the generation of a variety of autoantibodies against the self, SLE is the only disease to qualify. Identification of [...] Read more.
SLE is characterized by the generation of a variety of autoantibodies including anti-dsDNA autoantibodies, causing damage in various organs. If autoimmunity is defined by the generation of a variety of autoantibodies against the self, SLE is the only disease to qualify. Identification of the SLE-causing factor must fulfill the following criteria: (i) the factor induces SLE, (ii) the factor is operating in active SLE and (iii) SLE heals after removal of the factor. All candidate factors are reviewed from this viewpoint in this review. As to the cause of SLE, high levels of interferon α can induce SLE; however, interferon α in most patients did not reach this high level. BAFF (B cell activating factor of the TNF family) is increased in SLE. BAFF itself induced some manifestation of SLE, whereas removal of interferon α or BAFF by an antibody (Ab) did not heal SLE. BXSB male mice with a duplicated TLR7 gene develop SLE; however, the gene Sle1 is also required for the development of SLE. In addition, sanroque mice develop a variety of autoantibodies and SLE; the sanroque mutation, which disrupts one of the repressors of ICOS, results in increased CCR7lo CXCR5+Tfh cells, IL-21 and SLE. ICOS+T follicular helper (Tfh) cells increase in SLE and SLE-model (NZBxNZW)F1 mice, and the blockade of Tfh development ameliorated SLE, indicating the importance of Tfh cells in the pathogenesis of SLE. Self-organized criticality theory shows that SLE is caused by repeated infection, wherein SLE-inducing pathogens can vary individually depending on one’s HLA; however, the pathogen presented on HLA stimulates the T cell receptor (TCR) strongly beyond self-organized criticality. This stimulation generates TCR-revised, autoreactive DOCK8+Tfh cells, which induced a variety of autoantibodies and SLE. The SARS-CoV-2 virus is an example pathogen because SLE occurs after SARS-CoV-2 infection and vaccination. DOCK8+Tfh cells and SLE decreased after conventional or anti-DOCK Ab therapies. Thus, DOCK8+Tfh cells newly generated after repeated infection fulfill the criteria (i), (ii) and (iii) as the cause of SLE. Full article
(This article belongs to the Special Issue Molecular Insights into Systemic Lupus Erythematosus Pathogenesis: From Genes to Immune Signaling)
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