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Pathophysiology
Special Issues
Pathophysiology of Autoimmune Diseases
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Pathophysiology of Autoimmune Diseases

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

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 22145

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
Prof. Dr. Yehuda Shoenfeld

grade E-Mail Website
Guest Editor
1. Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat Gan 52621, Israel
2. Laboratory of the Mosaics of Autoimmunity, Saint Petersburg State University, 199034 Saint-Petersburg, Russia
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. Dr. Yehuda Shoenfeld
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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
  • 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

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Published Papers (4 papers)

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Research

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17 pages, 8662 KiB  
Article
SARS-CoV-2-Induced Pathology—Relevance to COVID-19 Pathophysiology
by Vsevolod A. Zinserling, Natalia Yu Semenova, Anastasia E. Bikmurzina, Natalia M. Kruglova, Oksana V. Rybalchenko and Alexander G. Markov
Pathophysiology 2022, 29(2), 281-297; https://doi.org/10.3390/pathophysiology29020021 - 10 Jun 2022
Cited by 5 | Viewed by 2786
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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Review

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8 pages, 3368 KiB  
Review
Corneal Confocal Microscopy in the Diagnosis of Small Fiber Neuropathy: Faster, Easier, and More Efficient Than Skin Biopsy?
by Mariia V. Lukashenko, Natalia Y. Gavrilova, Anna V. Bregovskaya, Lidiia A. Soprun, Leonid P. Churilov, Ioannis N. Petropoulos, Rayaz A Malik and Yehuda Shoenfeld
Pathophysiology 2022, 29(1), 1-8; https://doi.org/10.3390/pathophysiology29010001 - 26 Dec 2021
Cited by 12 | Viewed by 4048
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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31 pages, 6066 KiB  
Review
The Role of Exposomes in the Pathophysiology of Autoimmune Diseases I: Toxic Chemicals and Food
by Aristo Vojdani and Elroy Vojdani
Pathophysiology 2021, 28(4), 513-543; https://doi.org/10.3390/pathophysiology28040034 - 18 Dec 2021
Cited by 17 | Viewed by 9169
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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Other

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5 pages, 242 KiB  
Hypothesis
The Usefulness of Rare Blood Group Systems in the Risk Determination for Severe COVID-19
by Theocharis G. Konstantinidis, Valeria Iliadi, Georges Martinis and Maria Panopoulou
Pathophysiology 2021, 28(4), 496-500; https://doi.org/10.3390/pathophysiology28040032 - 3 Nov 2021
Cited by 1 | Viewed by 2906
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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