Mosaic of Autoimmunity

A special issue of Pathophysiology (ISSN 1873-149X).

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 16719

Special Issue Editors


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Guest Editor
Laboratory of the Mosaic of Autoimmunity, Saint Petersburg State University, 199034 Saint Petersburg, Russia
Interests: pathophysiology; experimental medicine; immunology; history of medicine; endocrine and metabolic disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The development of autoimmune diseases is multifactorial and subordinated to laws of the additive polygenetic inheritance with the threshold effect from the side of a whole series of natural and sociocultural anthropogenic epigenetic factors, sometimes even including iatrogenic ones. Since the autoimmune diseases of different organs and systems have much in common considering their pathophysiology, clinical manifestations, prevention, and treatment approaches, a new interdisciplinary branch of medicine—autoimmunology—has formed recently in front of our eyes. About 90 autoimmune diseases have been described, which implicate all organs and systems and belong to the sphere of all medical specializations. The global prevalence of autoimmune diseases is steadily growing. There is strong evidence for the existence of autoimmune/autoinflammatory links in the pathogenesis of COVID-19 and post-COVID syndrome. Although there is considerable progress in autoimmunity research, the nature of the general disturbances, which underlie various particular forms of autoimmune disorders, remains the urgent object of scientific studies and a hot topic of discussion. At the same time, practical healthcare worldwide experiences the utmost need for prophylaxis targets and effective modalities of autoimmune disorder treatment and the minimization of their adverse effects. The evolution of nature and the development of civilization has set many new challenges for biomedical science and for healthcare systems, including new risk factors for autoimmune diseases; hence, there is a great possibility that the 21st century will turn into an aeon of autoimmunity.

 In the presence of primary individual hereditary predisposition, pathological autoimmunity can manifest differently under the influence of various exogenous adjuvants or, vice versa—immunosuppressive factors—interplaying at different life periods of an individual, while autoimmune disorders in the human body seem to flow from one nosological entity to another, keeping a similar background, which is a principle known as the “kaleidoscope of autoimmunity”. After the success of the first Special Issue of Pathophysiology [2022, 29(2)] dedicated to autoimmunity problems, we launch the new Special Issue, entitled “Mosaic of Autoimmunity”, which aims to attract both researchers and clinicians of various specialties, and contributions from leading scholars in this scientific area.

We invite you to submit reviews, original papers, and case reports with pathophysiological commentaries.

Dr. Leonid Churilov
Prof. Dr. Yehuda Shoenfeld
Guest Editors

Manuscript Submission Information

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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. Pathophysiology is an international peer-reviewed open access quarterly 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 1400 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

  • autoimmunity
  • autoimmune diseases
  • aetiology
  • pathogenesis
  • models
  • experimental therapy
  • geoepidemiology
  • adjuvants
  • ASIA syndrome
  • dysautonomia
  • infertility
  • adverse effects of checkpoint inhibitor therapy
  • functional antibodies
  • physiologic autoimmunity
  • autoimmunity and microbiota
  • autoimmunity and cancer
  • autoimmunity and vaccines
  • COVID-19 and autoimmunity cardiovascular diseases
  • arteries
  • vasodilation
  • blood pressure
  • prostacyclin
  • nitric oxide
  • adenosine
  • hyperpolarization
  • polyphenolic substances
  • nanoparticles

Published Papers (5 papers)

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Research

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9 pages, 1709 KiB  
Article
Molecular Mimicry between SARS-CoV-2 and Human Endocrinocytes: A Prerequisite of Post-COVID-19 Endocrine Autoimmunity?
by Leonid P. Churilov, Muslimbek G. Normatov and Vladimir J. Utekhin
Pathophysiology 2022, 29(3), 486-494; https://doi.org/10.3390/pathophysiology29030039 - 25 Aug 2022
Cited by 20 | Viewed by 3218
Abstract
Molecular mimicry between human and microbial/viral/parasite peptides is common and has long been associated with the etiology of autoimmune disorders provoked by exogenous pathogens. A growing body of evidence accumulated in recent years suggests a strong correlation between SARS-CoV-2 infection and autoimmunity. The [...] Read more.
Molecular mimicry between human and microbial/viral/parasite peptides is common and has long been associated with the etiology of autoimmune disorders provoked by exogenous pathogens. A growing body of evidence accumulated in recent years suggests a strong correlation between SARS-CoV-2 infection and autoimmunity. The article analyzes the immunogenic potential of the peptides shared between the SARS-CoV-2 spike glycoprotein (S-protein) and antigens of human endocrinocytes involved in most common autoimmune endocrinopathies. A total of 14 pentapeptides shared by the SARS-CoV-2 S-protein, thyroid, pituitary, adrenal cortex autoantigens and beta-cells of the islets of Langerhans were identified, all of them belong to the immunoreactive epitopes of SARS-CoV-2. The discussion of the findings relates the results to the clinical correlates of COVID-19-associated autoimmune endocrinopathies. The most common of these illnesses is an autoimmune thyroid disease, so the majority of shared pentapeptides belong to the marker autoantigens of this disease. The most important in pathogenesis of severe COVID-19, according to the authors, may be autoimmunity against adrenals because their adequate response prevents excessive systemic action of the inflammatory mediators causing cytokine storm and hemodynamic shock. A critique of the antigenic mimicry concept is given with an assertion that peptide sharing is not a guarantee but only a prerequisite for provoking autoimmunity based on the molecular mimicry. The latter event occurs in carriers of certain HLA haplotypes and when a shared peptide is only used in antigen processing Full article
(This article belongs to the Special Issue Mosaic of Autoimmunity)
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16 pages, 2228 KiB  
Article
Heart Dysfunction in Essential Hypertension Depends on Systemic Proinflammatory Influences: A Retrospective Clinical Pathophysiological Study
by Anton V. Barsukov, Alexander E. Korovin, Leonid P. Churilov, Ekaterina V. Borisova and Dmitry V. Tovpeko
Pathophysiology 2022, 29(3), 453-468; https://doi.org/10.3390/pathophysiology29030036 - 7 Aug 2022
Cited by 3 | Viewed by 1959
Abstract
Low-intensity systemic inflammation is an important element of heart failure pathogenesis. The aim of this study is to assess proinflammatory status serum indicators (C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6)) in middle-aged males (M) and females (F) with essential hypertension [...] Read more.
Low-intensity systemic inflammation is an important element of heart failure pathogenesis. The aim of this study is to assess proinflammatory status serum indicators (C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6)) in middle-aged males (M) and females (F) with essential hypertension (HTN) depending on left ventricular (LV) diastolic dysfunction (LVDD). The main group comprised 55 M and 49 F with the first- to second-severity grade HTN with mild heart failure and a preserved LV ejection fraction ≥50%. Patients had sinus rhythm, first or second-severity degree LVDD, LV hypertrophy, left atrium dilatation, and NT-proBNP > 125 pg/mL. Comparison group: 30 hypertensives without cardiac dysfunction; control group: 31 normotensives. Quantitative features were compared using the Mann–Whitney test, median χ2, ANOVA module. Spearman’s rank correlation coefficients were determined to identify the relationship between the proinflammatory pattern and exercise tolerance. Hypertensive M had markedly higher CRP, TNF-α, and IL-6 levels compared to F. All mean values corresponded to reference range. In patients with second-degree LVDD, CRP, TNF-α, and IL-6 levels were significantly greater than in subjects with first-degree LVDD (both within M and within F samples). Significant negative associations between CRP, IL-6, and TNF-α levels and the 6 min walk test existed in hypertensive M and F. The study demonstrated a close relationship between the proinflammatory pattern and LVDD and exercise tolerance indicators, regardless of the hypertensive patient’s sex. Full article
(This article belongs to the Special Issue Mosaic of Autoimmunity)
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Review

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14 pages, 1534 KiB  
Review
Current Views about the Inflammatory Damage Triggered by Bacterial Superantigens and Experimental Attempts to Neutralize Superantigen-Mediated Toxic Effects with Natural and Biological Products
by Luigi Santacroce, Skender Topi, Ioannis Alexandros Charitos, Roberto Lovero, Paolo Luperto, Raffaele Palmirotta and Emilio Jirillo
Pathophysiology 2024, 31(1), 18-31; https://doi.org/10.3390/pathophysiology31010002 - 9 Jan 2024
Cited by 1 | Viewed by 1416
Abstract
Superantigens, i.e., staphylococcal enterotoxins and toxic shock syndrome toxin-1, interact with T cells in a different manner in comparison to conventional antigens. In fact, they activate a larger contingent of T lymphocytes, binding outside the peptide-binding groove of the major histocompatibility complex class [...] Read more.
Superantigens, i.e., staphylococcal enterotoxins and toxic shock syndrome toxin-1, interact with T cells in a different manner in comparison to conventional antigens. In fact, they activate a larger contingent of T lymphocytes, binding outside the peptide-binding groove of the major histocompatibility complex class II. Involvement of many T cells by superantigens leads to a massive release of pro-inflammatory cytokines, such as interleukin (IL)-1, IL-2, IL-6, tumor necrosis factor-alpha and interferon-gamma. Such a storm of mediators has been shown to account for tissue damage, multiorgan failure and shock. Besides conventional drugs and biotherapeutics, experiments with natural and biological products have been undertaken to attenuate the toxic effects exerted by superantigens. In this review, emphasis will be placed on polyphenols, probiotics, beta-glucans and antimicrobial peptides. In fact, these substances share a common functional denominator, since they skew the immune response toward an anti-inflammatory profile, thus mitigating the cytokine wave evoked by superantigens. However, clinical applications of these products are still scarce, and more trials are needed to validate their usefulness in humans. Full article
(This article belongs to the Special Issue Mosaic of Autoimmunity)
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30 pages, 5631 KiB  
Review
Biomolecular Mechanisms of Autoimmune Diseases and Their Relationship with the Resident Microbiota: Friend or Foe?
by Skender Topi, Lucrezia Bottalico, Ioannis Alexandros Charitos, Marica Colella, Marina Di Domenico, Raffaele Palmirotta and Luigi Santacroce
Pathophysiology 2022, 29(3), 507-536; https://doi.org/10.3390/pathophysiology29030041 - 1 Sep 2022
Cited by 11 | Viewed by 3002
Abstract
The use of innovative approaches to elucidate the pathophysiological mechanisms of autoimmune diseases, as well as to further study of the factors which can have either a positive or negative effect on the course of the disease, is essential. In this line, the [...] Read more.
The use of innovative approaches to elucidate the pathophysiological mechanisms of autoimmune diseases, as well as to further study of the factors which can have either a positive or negative effect on the course of the disease, is essential. In this line, the development of new molecular techniques and the creation of the Human Genome Program have allowed access to many more solutions to the difficulties that exist in the identification and characterization of the microbiome, as well as changes due to various factors. Such innovative technologies can rekindle older hypotheses, such as molecular mimicry, allowing us to move from hypothesis to theory and from correlation to causality, particularly regarding autoimmune diseases and dysbiosis of the microbiota. For example, Prevotella copri appears to have a strong association with rheumatoid arthritis; it is expected that this will be confirmed by several scientists, which, in turn, will make it possible to identify other mechanisms that may contribute to the pathophysiology of the disease. This article seeks to identify new clues regarding similar correlations between autoimmune activity and the human microbiota, particularly in relation to qualitative and quantitative microbial variations therein. Full article
(This article belongs to the Special Issue Mosaic of Autoimmunity)
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12 pages, 888 KiB  
Review
Autoimmune Autonomic Dysfunction Syndromes: Potential Involvement and Pathophysiology Related to Complex Regional Pain Syndrome, Fibromyalgia, Chronic Fatigue Syndrome, Silicone Breast Implant–Related Symptoms and Post-COVID Syndrome
by Naim Mahroum and Yehuda Shoenfeld
Pathophysiology 2022, 29(3), 414-425; https://doi.org/10.3390/pathophysiology29030033 - 28 Jul 2022
Cited by 11 | Viewed by 6075
Abstract
The pathophysiological mechanisms involved in chronic disorders such as complex regional pain syndrome, fibromyalgia, chronic fatigue syndrome, silicone breast implant–related symptoms, and post-COVID syndrome have not been clearly defined. The course of the pain in some of the syndromes, the absence of evident [...] Read more.
The pathophysiological mechanisms involved in chronic disorders such as complex regional pain syndrome, fibromyalgia, chronic fatigue syndrome, silicone breast implant–related symptoms, and post-COVID syndrome have not been clearly defined. The course of the pain in some of the syndromes, the absence of evident tissue damage, and the predominance of alterations in the autonomic nervous system are shared similarities between them. The production of autoantibodies following a trigger in the syndromes was previously described, for instance, trauma in complex regional pain syndrome, infectious agents in fibromyalgia, chronic fatigue syndrome, and post-COVID syndrome, and the immune stimulation by silicone in women with breast implants. In fact, the autoantibodies produced were shown to be directed against the autonomic nervous system receptors, leading to the amplification of the perception of pain alongside various clinical symptoms seen during the clinical course of the syndromes. Therefore, we viewed autoantibodies targeting the autonomic nervous system resulting in autonomic dysfunction as likely the most comprehensive explanation of the pathophysiology of the disorders mentioned. Based on this, we aimed to introduce a new concept uniting complex regional pain syndrome, fibromyalgia, chronic fatigue syndrome, silicone breast implant–related symptoms, and post-COVID syndrome, namely “autoimmune autonomic dysfunction syndromes”. Due to its etiological, pathophysiological, and clinical implications, the suggested term would be more precise in classifying the syndromes under one title. The new title would doubtlessly facilitate both laboratory and clinical studies aimed to improve diagnosis and make treatment options more directed and precise. Full article
(This article belongs to the Special Issue Mosaic of Autoimmunity)
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