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Advances in Molecular Research on Autoimmune Diseases, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 25 November 2024 | Viewed by 1323

Special Issue Editor


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Guest Editor
1. Department of Neurology, Juntendo University, Tokyo 1138421, Japan
2. Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy
Interests: experimental autoimmune encephalomyelitis; multiple sclerosis; autoimmunity; neuroimmunology; microbiology; neurodegeneration; astrocytes; mycobacteria; BCG
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Special Issue Information

Dear Colleagues,

Autoimmune diseases are a group of disorders characterized by the immune system mistakenly attacking healthy cells and tissues in the body. These conditions can affect various organs, including the central and peripheral nervous systems, leading to significant morbidity and an impaired quality of life.

Understanding the role of genetic predisposition, environmental triggers and dysregulated immune responses has provided valuable insights into the development of autoimmune diseases. Genetic studies have highlighted numerous susceptibility genes, emphasizing the intricate interplay between genetic factors and environmental influences.

Efforts have been directed toward unraveling the immunological pathways involved in autoimmune diseases. Technological advances and the use of animal models have allowed for the identification of specific immune cells as key players in disease pathogenesis. Additionally, the discovery of autoantibodies and their targeting of self-antigens has provided important diagnostic and prognostic markers for several autoimmune disorders.

Novel therapeutic approaches have emerged aiming to modulate or suppress the aberrant immune responses seen in autoimmune diseases. Immune-modulating drugs, biologics and cell-based therapies have shown promising results in managing these conditions.

This Special Issue welcomes contributions that focus on recent advances in autoimmune disease research, with the aim of shedding light on the underlying mechanisms of these complex disorders and exploring potential therapeutic strategies.

Dr. Davide Cossu
Guest Editor

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Keywords

  • autoimmune markers
  • immunology
  • pathogenesis
  • immunogenetics
  • animal models
  • immunotherapy

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Published Papers (1 paper)

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Research

12 pages, 2828 KiB  
Article
NRF2 Plays a Crucial Role in the Tolerogenic Effect of Ethyl Pyruvate on Dendritic Cells
by Suzana Stanisavljević, Goran Stegnjaić, Bojan Jevtić, Mirjana Dimitrijević, Đorđe Miljković, Irena Lavrnja and Neda Nikolovski
Int. J. Mol. Sci. 2024, 25(11), 6195; https://doi.org/10.3390/ijms25116195 - 4 Jun 2024
Viewed by 932
Abstract
Ethyl pyruvate (EP) is a redox-active compound that has been previously shown to be effective in restraining immune hyperactivity in animal models of various autoimmune and chronic inflammatory diseases. Importantly, EP has also been proven to have a potent tolerogenic effect on dendritic [...] Read more.
Ethyl pyruvate (EP) is a redox-active compound that has been previously shown to be effective in restraining immune hyperactivity in animal models of various autoimmune and chronic inflammatory diseases. Importantly, EP has also been proven to have a potent tolerogenic effect on dendritic cells (DCs). Here, the influence of EP on the signaling pathways in DCs relevant for their tolerogenicity, including anti-inflammatory NRF2 and pro-inflammatory NF-κB, was explored. Specifically, the effects of EP on DCs obtained by GM-CSF-directed differentiation of murine bone marrow precursor cells and matured under the influence of lipopolysaccharide (LPS) were examined via immunocytochemistry and RT-PCR. EP counteracted LPS-imposed morphological changes and down-regulated the LPS-induced expression of pro-inflammatory mediators in DCs. While it reduced the activation of NF-κB, EP potentiated NRF2 and downstream antioxidative molecules, thus implying the regulation of NRF2 signaling pathways as the major reason for the tolerizing effects of EP on DCs. Full article
(This article belongs to the Special Issue Advances in Molecular Research on Autoimmune Diseases, 2nd Edition)
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