Special Issue "Pathophysiology of Autoimmune Diseases"

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

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 20119

Special Issue Editors

Dr. Leonid Churilov
E-Mail Website
Guest Editor
Research Institute of Phthisiopulmonology, Saint Petersburg State University; Saint Petersburg, Russia
Interests: 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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Yehuda Shoenfeld
grade E-Mail Website
Guest Editor
Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Aviv University, Israel; Laboratory of the Mosaics of Autoimmunity, Saint Petersburg State University, Saint-Petersburg, Russian
Interests: clinical immunology; autoimmune diseases; rheumatology diseases; lupus
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, as well as their 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. Autoimmune diseases’ morbidity and mortality steadily grow in all developed countries. There is strong evidence for existence of autoimmune/autoinflammatory links in the pathogenesis of severe COVID-19 cases of current global pandemic. In spite of the successes in the study of the etiology, pathogenesis, and models of many autoimmune illnesses, the nature of the general disturbances, which underlie various particular forms of autoimmune disorders, remains the urgent object of scientific studies and discussions. At the same time, practical healthcare worldwide experiences the utmost need for target prophylaxis and effective modalities of autoimmune disorder treatment, and minimization of their adverse effects. The evolution of nature and development of civilization set many new challenges for biomedical science and for healthcare systems, including new risk factors of autoimmune diseases; hence, there is a great possibility that the 21st century will turn into an aeon of autoimmunity.

This trend may in future change the whole philosophy of clinical medicine. Currently, it is believed that autoimmune diseases are induced through a combination of genetic and environmental factors. The genotype distinguishes individuals who may possess inherited characteristics, making their immune system hyperactive (e.g., HLA DRb1). The environmental factors include, first of all, those compounds that have an adjuvant effect (from the Latin word adjuvare—“to help or aid”). This means that such a factor may enhance immune responses modifying the immunoregulating interactions. 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 a concrete person, 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”. The Special Issue of Pathophysiology dedicated to autoimmunity problems aims to attract both researchers and clinicians of various specialties and contributions by leading scholars of this scientific area.

Dr. Leonid Churilov
Prof. Yehuda Shoenfeld
Guest Editors

Manuscript Submission Information

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Keywords

  • autoimmunity
  • autoimmune diseases
  • etiology
  • 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 (8 papers)

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Research

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Article
SARS-CoV-2-Induced Pathology—Relevance to COVID-19 Pathophysiology
Pathophysiology 2022, 29(2), 281-297; https://doi.org/10.3390/pathophysiology29020021 - 10 Jun 2022
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Abstract
In spite of intensive studies of different aspects of a new coronavirus infection, many issues still remain unclear. In a screening analysis of histopathology in l200 lethal cases, authors succeeded in performing a wide spectrum of immune histochemical reactions (CD2, CD 3, CD [...] Read more.
In spite of intensive studies of different aspects of a new coronavirus infection, many issues still remain unclear. In a screening analysis of histopathology in l200 lethal cases, authors succeeded in performing a wide spectrum of immune histochemical reactions (CD2, CD 3, CD 4, CD 5, CD 7, CD 8, CD14, CD 20, CD 31, CD 34, CD 56, CD 57, CD 68, CD 163, collagen 1,3, spike protein SARS-CoV-2, caspase-3, MLCM; ACE2 receptor, occludin, and claudin-1 and -3) and electron microscopy. The results of the histological and IHC studies of deceased people with varying degrees of severity of coronavirus infection confirmed the ability of these pathogens to cause cytoproliferative changes, primarily in epithelial and endothelial cells. Lesions of various organs are possible, while the reasons for significant differences in organotropy remain unclear. Severe respiratory failure in COVID-19 in humans is associated with a very peculiar viral pneumonia. In the pathogenesis of COVID-19, the most important role is played by lesions of the microcirculatory bed, the genesis of which requires further study, but direct viral damage is most likely. Endothelial damage can be associated with both thrombosis in vessels of various calibers, leading to characteristic complications, and the development of DIC syndrome with maximal kidney damage. Such lesions can be the basis of clinically diagnosed septic shock, while usually there are no morphological data in favor of classical sepsis caused by bacteria or fungi. A massive infiltration of the lung tissue and other organs, mainly by T lymphocytes, including those with suppressor properties, makes it necessary to conduct a differential diagnosis between the morphological manifestation of the protective cellular immune response and direct viral lesions but does not exclude the hypothesis of an immunopathological component of pathogenesis. In many of the deceased, even in the absence of clear clinical symptoms, a variety of extrapulmonary lesions were also detected. The mechanism of their development probably has a complex nature: direct lesions associated with the generalization of viral infection and vascular disorders associated with endothelial damage and having an autoimmune nature. Many aspects of the pathogenesis of coronavirus infection require further comprehensive study. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Article
Chronic Fatigue Exhibits Heterogeneous Autoimmunity Characteristics Which Reflect Etiology
Pathophysiology 2022, 29(2), 187-199; https://doi.org/10.3390/pathophysiology29020016 - 25 May 2022
Cited by 1 | Viewed by 1895
Abstract
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is considered to be associated with post-viral complications and mental stress, but the role of autoimmunity also remains promising. A comparison of autoimmune profiles in chronic fatigue of different origin may bring insights on the pathogenesis of this [...] Read more.
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is considered to be associated with post-viral complications and mental stress, but the role of autoimmunity also remains promising. A comparison of autoimmune profiles in chronic fatigue of different origin may bring insights on the pathogenesis of this disease. Thirty-three patients with CFS/ME were divided into three subgroups. The first group included Herpesviridae carriers (group V), the second group included stress-related causes of chronic fatigue (distress, group D), and the third group included idiopathic CFS/ME (group I). Were evaluated thirty-six neural and visceral autoantigens with the ELISA ELI-test (Biomarker, Russia) and compared to 20 healthy donors, either without any fatigue (group H), or “healthy but tired” (group HTd) with episodes of fatigue related to job burnout not fitting the CFS/ME criteria. β2-glycoprotein-I autoantibodies were increased in CFS/ME patients, but not in healthy participants, that alludes the link between CFS/ME and antiphospholipid syndrome (APS) earlier suspected by Berg et al. (1999). In CFS/ME patients, an increase in levels of autoantibodies towards the non-specific components of tissue debris (double-stranded DNA, collagen) was shown. Both CFS and HTd subgroups had elevated level of autoantibodies against serotonin receptors, glial fibrillary acidic protein and protein S100. Only group V showed an elevation in the autoantibodies towards voltage-gated calcium channels, and only group D had elevated levels of dopamine-, glutamate- and GABA-receptor autoantibodies, as well as NF200-protein autoantibodies. Therefore, increased autoimmune reactions to the multiple neural antigens and to adrenal medullar antigen, but not to other tissue-specific somatic ones were revealed. An increase in autoantibody levels towards some neural and non-tissue-specific antigens strongly correlated with a CFS/ME diagnosis. Autoimmune reactions were described in all subtypes of the clinically significant chronic fatigue. Visceral complaints in CFS/ME patients may be secondary to the neuroendocrine involvement and autoimmune dysautonomia. CFS may be closely interrelated with antiphospholipid syndrome, that requires further study. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Article
New Clinical Phenotype of the Post-Covid Syndrome: Fibromyalgia and Joint Hypermobility Condition
Pathophysiology 2022, 29(1), 24-29; https://doi.org/10.3390/pathophysiology29010003 - 19 Jan 2022
Cited by 4 | Viewed by 4589
Abstract
Fibromyalgia can be defined as a chronic pain condition, affecting the musculoskeletal system, etiology and pathophysiology of which is sufficiently understudied. Despite the fact that many authors consider this entity to be a manifestation of central sensitization, and not an autoimmune disease, the [...] Read more.
Fibromyalgia can be defined as a chronic pain condition, affecting the musculoskeletal system, etiology and pathophysiology of which is sufficiently understudied. Despite the fact that many authors consider this entity to be a manifestation of central sensitization, and not an autoimmune disease, the high prevalence of fibromyalgia in patients with post-COVID-19 conditions requires taking a fresh look at the causes of the disease development. During the patient examination, the authors identified a combination of symptoms that occurs so often, that they can be carefully described as a clinical pattern. These manifestations include young age, female gender, joint hypermobility, the onset of pain after COVID-19, physical traumatization of one particular tendon and the development of the fibromyalgia pain syndrome during the next several weeks. As well as an increase in the titer of antinuclear antibodies and some other systemic inflammation factors. It can be assumed with great caution that local damage to the connective tissue in patients with joint hypermobility, having COVID-19 as a trigger factor can lead to the development of fibromyalgia syndrome. This article presents three clinical cases that illustrated this hypothesis. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)

Review

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Review
The Role of Exposomes in the Pathophysiology of Autoimmune Diseases II: Pathogens
Pathophysiology 2022, 29(2), 243-280; https://doi.org/10.3390/pathophysiology29020020 - 03 Jun 2022
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Abstract
In our continuing examination of the role of exposomes in autoimmune disease, we use this review to focus on pathogens. Infections are major contributors to the pathophysiology of autoimmune diseases through various mechanisms, foremost being molecular mimicry, when the structural similarity between the [...] Read more.
In our continuing examination of the role of exposomes in autoimmune disease, we use this review to focus on pathogens. Infections are major contributors to the pathophysiology of autoimmune diseases through various mechanisms, foremost being molecular mimicry, when the structural similarity between the pathogen and a human tissue antigen leads to autoimmune reactivity and even autoimmune disease. The three best examples of this are oral pathogens, SARS-CoV-2, and the herpesviruses. Oral pathogens reach the gut, disturb the microbiota, increase gut permeability, cause local inflammation, and generate autoantigens, leading to systemic inflammation, multiple autoimmune reactivities, and systemic autoimmunity. The COVID-19 pandemic put the spotlight on SARS-CoV-2, which has been called “the autoimmune virus.” We explore in detail the evidence supporting this. We also describe how viruses, in particular herpesviruses, have a role in the induction of many different autoimmune diseases, detailing the various mechanisms involved. Lastly, we discuss the microbiome and the beneficial microbiota that populate it. We look at the role of the gut microbiome in autoimmune disorders, because of its role in regulating the immune system. Dysbiosis of the microbiota in the gut microbiome can lead to multiple autoimmune disorders. We conclude that understanding the precise roles and relationships shared by all these factors that comprise the exposome and identifying early events and root causes of these disorders can help us to develop more targeted therapeutic protocols for the management of this worldwide epidemic of autoimmunity. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Review
Corneal Confocal Microscopy in the Diagnosis of Small Fiber Neuropathy: Faster, Easier, and More Efficient Than Skin Biopsy?
Pathophysiology 2022, 29(1), 1-8; https://doi.org/10.3390/pathophysiology29010001 - 26 Dec 2021
Cited by 1 | Viewed by 2296
Abstract
Chronic pain may affect 30–50% of the world’s population and an important cause is small fiber neuropathy (SFN). Recent research suggests that autoimmune diseases may be one of the most common causes of small nerve fiber damage. There is low awareness of SFN [...] Read more.
Chronic pain may affect 30–50% of the world’s population and an important cause is small fiber neuropathy (SFN). Recent research suggests that autoimmune diseases may be one of the most common causes of small nerve fiber damage. There is low awareness of SFN among patients and clinicians and it is difficult to diagnose as routine electrophysiological methods only detect large fiber abnormalities, and specialized small fiber tests, like skin biopsy and quantitative sensory testing, are not routinely available. Corneal confocal microscopy (CCM) is a rapid, non-invasive, reproducible method for quantifying small nerve fiber degeneration and regeneration, and could be an important tool for diagnosing SFN. This review considers the advantages and disadvantages of CCM and highlights the evolution of this technique from a research tool to a diagnostic test for small fiber damage, which can be a valuable contribution to the study and management of autoimmune disease. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Review
The Role of Exposomes in the Pathophysiology of Autoimmune Diseases I: Toxic Chemicals and Food
Pathophysiology 2021, 28(4), 513-543; https://doi.org/10.3390/pathophysiology28040034 - 18 Dec 2021
Cited by 5 | Viewed by 2771
Abstract
Autoimmune diseases affect 5–9% of the world’s population. It is now known that genetics play a relatively small part in the pathophysiology of autoimmune disorders in general, and that environmental factors have a greater role. In this review, we examine the role of [...] Read more.
Autoimmune diseases affect 5–9% of the world’s population. It is now known that genetics play a relatively small part in the pathophysiology of autoimmune disorders in general, and that environmental factors have a greater role. In this review, we examine the role of the exposome, an individual’s lifetime exposure to external and internal factors, in the pathophysiology of autoimmune diseases. The most common of these environmental factors are toxic chemicals, food/diet, and infections. Toxic chemicals are in our food, drink, common products, the air, and even the land we walk on. Toxic chemicals can directly damage self-tissue and cause the release of autoantigens, or can bind to human tissue antigens and form neoantigens, which can provoke autoimmune response leading to autoimmunity. Other types of autoimmune responses can also be induced by toxic chemicals through various effects at the cellular and biochemical levels. The food we eat every day commonly has colorants, preservatives, or packaging-related chemical contamination. The food itself may be antigenic for susceptible individuals. The most common mechanism for food-related autoimmunity is molecular mimicry, in which the food’s molecular structure bears a similarity with the structure of one or more self-tissues. The solution is to detect the trigger, remove it from the environment or diet, then repair the damage to the individual’s body and health. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Review
Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine, and Endocrine Dysregulation
Pathophysiology 2021, 28(4), 471-488; https://doi.org/10.3390/pathophysiology28040030 - 15 Oct 2021
Cited by 2 | Viewed by 2187
Abstract
According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility is often associated with autoimmunity towards sperm antigens essential for fertilization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and [...] Read more.
According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility is often associated with autoimmunity towards sperm antigens essential for fertilization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and acrosomal reaction, and thus preventing ovum fertilization. Infertility diagnosis requires a mandatory check for the ASAs. The concept of the blood–testis barrier is currently re-formulated, with an emphasis on informational paracrine and juxtacrine effects, rather than simple anatomical separation. The etiology of male infertility includes both autoimmune and non-autoimmune diseases but equally develops through autoimmune links of pathogenesis. Varicocele commonly leads to infertility due to testicular ischemic damage, venous stasis, local hyperthermia, and hypoandrogenism. However, varicocelectomy can alter the blood–testis barrier, facilitating ASAs production as well. There are contradictory data on the role of ASAs in the pathogenesis of varicocele-related infertility. Infection and inflammation both promote ASAs production due to “danger concept” mechanisms and because of antigen mimicry. Systemic pro-autoimmune influences like hyperprolactinemia, hypoandrogenism, and hypothyroidism also facilitate ASAs production. The diagnostic value of various ASAs has not yet been clearly attributed, and their cut-levels have not been determined in sera nor in ejaculate. The assessment of the autoimmunity role in the pathogenesis of male infertility is ambiguous, so the purpose of this review is to show the effects of ASAs on the pathogenesis of male infertility. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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Other

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Hypothesis
The Usefulness of Rare Blood Group Systems in the Risk Determination for Severe COVID-19
Pathophysiology 2021, 28(4), 496-500; https://doi.org/10.3390/pathophysiology28040032 - 03 Nov 2021
Cited by 1 | Viewed by 1801
Abstract
The newly identified human coronavirus was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), based on a detailed analysis of clinical manifestation. It was reported that blood type O individuals were less likely to become infected by SARS-CoV, while blood type A individuals [...] Read more.
The newly identified human coronavirus was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), based on a detailed analysis of clinical manifestation. It was reported that blood type O individuals were less likely to become infected by SARS-CoV, while blood type A individuals have an increased risk of severe illness. The Forssman antigen, or Forssman glycolipid synthase (FS), was first described in 1911 by John Frederick Forssman. Blood type A/B glycosyltransferases (AT/BTs) and Forssman glycolipid synthase (FS) are encoded by the evolutionarily related ABO (A/B alleles) and GBGT1 genes. In this article, based on published studies about the pathogenesis of the COVID-19, we hypothesize the possible relationship between the COVID-19 infection and rare blood type systems, such as the Forssman antigen system. Full article
(This article belongs to the Special Issue Pathophysiology of Autoimmune Diseases)
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