Autoimmune diseases result from a combination of genetic and environmental factors that disrupt normal immune responses to infections while also preventing autoimmune reactions (, ). Genes governing antigen detection, processing, and lymphocyte interactions play a crucial role among genetic factors (). Among environmental factors, infections and influences on immune system function are particularly significant (). The Epstein-Barr Virus (EBV) stands out, associated with various autoimmune diseases alongside its role in certain cancers (–). This association is supported by epidemiological data and an understanding of EBV’s immune evasion mechanisms (, ).
Within this Research Topic, Sharifinejad et al. analyze patients with monogenic combined immunodeficiencies, revealing autoimmune manifestations in about 18% of cases, often linked to mutations in immune system genes, highlighting the intricate link between immune deficiencies and autoimmunity.
Schönrich et al. discuss the central role of EBV in multiple sclerosis, focusing on the virally encoded IL-10 homologue and its impact on host IL-10 production, illustrating a significant immune evasion mechanism and its implications for central nervous system pathology.
The connection between immune system genes, infections, and autoimmunity is further explored by Xiao et al. in a meta-analysis of IFIH1 polymorphisms, showing positive correlations with type 1 diabetes, systemic lupus erythematosus, and multiple sclerosis.
Primary Sjögren’s Syndrome, a systemic autoimmune disease, is associated with B cell hyperactivity, lymphocyte infiltration, and destruction of exocrine glands, with potential links to EBV infection (, ). Hinrichs et al. demonstrate that SS patients exhibit distinct mucosa-associated invariant T (MAIT) cell behavior, expressing higher levels of certain markers that facilitate exocrine gland infiltration and pathology.
Dermatomyositis (DM), characterized by muscle weakness and rashes, may also be connected to immunodeficiency and infections (). Hilliard et al. show alterations in the natural killer (NK) cell population in juvenile DM, which could indicate impaired NK cell function.
Collectively, these articles underscore the intricate relationship between immunodeficiency, viral immune evasion mechanisms, and autoimmune conditions, offering valuable insights for the treatment and prevention of such diseases.
Statements
Author contributions
FR: Conceptualization, Resources, Visualization, Writing – review & editing, Methodology, Investigation. GH: Visualization, conceptualization, Writing – review & editing.
Acknowledgments
Many Thanks to the GH, Department of Neurology, Rigshospitalet, Research Park, Nordstjernevej 42, 2600 Glostrup, Denmark for his precious intellectual collaboration.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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Summary
Keywords
apoptosis, EBV, autoimmunity, disorders, drugs
Citation
Rizzo F and Houen G (2023) Editorial: Immune evasion mechanisms and their role in the pathogenesis of autoimmune disorders. Front. Immunol. 14:1267922. doi: 10.3389/fimmu.2023.1267922
Received
27 July 2023
Accepted
22 August 2023
Published
13 September 2023
Volume
14 - 2023
Edited and reviewed by
Betty Diamond, Feinstein Institute for Medical Research, United States
Updates
Copyright
© 2023 Rizzo and Houen.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Fabiana Rizzo, Fabiana.Rizzo@iss.it
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.