Special Issue "Autoimmune Diseases: Molecular and Cellular Mechanisms"

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: 31 July 2023 | Viewed by 763

Special Issue Editors

Division of Clinical Immunology at the Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden
Interests: immunogenetics; clinical immunology; immunotherapy; inborn errors of immunity; primary immunodeficiency
Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran
Interests: autoimmunity; autoinflammation; immune related disorders

Special Issue Information

Dear Colleagues,

The concomitant incidence of immunodeficiency and autoimmunity in early-onset patients may represent a paradox, yet it has been documented in an expanding number of conditions. The use of unbiased molecular studies to identify novel forms of inborn errors of immunity, along with in-depth functional studies of biological samples from affected cases, continues to clarify the novel pathogenesis underlying immune dysregulation and autoinflammation in patients with an altered central or peripheral tolerance, and contributes to fighting pathogens. The genetic etiology of autoimmune disease has the power to dramatically transform patient treatment, shifting clinical care from non-specific therapies to targeted therapies. The late onset of autoimmune disease in adult cases suggests that multiple genetic and non-genetic factors, including epigenetic alterations, contribute to disease pathogenesis. In this Special Issue, we welcome the submission of original research and review articles related to this topic.

Dr. Hassan Abolhassani
Dr. Gholamreza Azizi
Guest Editors

Manuscript Submission Information

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Keywords

  • autoimmunity
  • autoinflammation
  • immune dysregulation
  • inborn errors of immunity
  • primary immunodeficiency

Published Papers (1 paper)

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Research

Article
Reduced Renal CSE/CBS/H2S Contributes to the Progress of Lupus Nephritis
Biology 2023, 12(2), 318; https://doi.org/10.3390/biology12020318 - 16 Feb 2023
Viewed by 540
Abstract
The molecular mechanisms underlying lupus nephritis (LN) pathogenesis are not fully understood. Hydrogen sulfide (H2S) is involved in many pathological and physiological processes. We sought to investigate the roles of H2S in LN pathogenesis. H2S synthase cystathionine–lyase (CSE) and cystathionine–synthetase (CBS) expression was [...] Read more.
The molecular mechanisms underlying lupus nephritis (LN) pathogenesis are not fully understood. Hydrogen sulfide (H2S) is involved in many pathological and physiological processes. We sought to investigate the roles of H2S in LN pathogenesis. H2S synthase cystathionine–lyase (CSE) and cystathionine–synthetase (CBS) expression was downregulated in renal tissues of patients with LN and their levels were associated with LN’s prognosis using the Nephroseq database. Reduced CSE and CBS protein expression in kidney tissues of LN patients and MRL/lpr mice were confirmed by immunohistochemistry. CSE and CBS mRNA levels were reduced in MRL/lpr and pristine- and R848-induced lupus mice. Given that H2S exerts an anti-inflammatory role partly via regulating inflammatory transcription factors (TFs), we analyzed hub TFs by using a bioinformatics approach. It showed that STAT1, RELA, and T-cell-related signaling pathways were enriched in LN. Increased STAT1 and RELA expression were confirmed in renal tissues of LN patients. Treatment of MRL/lpr and pristine mice with H2S donors alleviated systemic lupus erythematosus (SLE) phenotypes and renal injury. H2S donors inhibited RELA level and T-cell infiltration in the kidneys of MRL/lpr and pristine mice. Our data indicated that CSE/CBS/H2S contributes to LN pathogenesis. Supplementation of H2S would be a potential therapeutic strategy for LN. Full article
(This article belongs to the Special Issue Autoimmune Diseases: Molecular and Cellular Mechanisms)
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