Let's learn where concerned!
Abstract
Notwithstanding the fact that the 12th international congress of autoimmunity (AUTO12) was held virtual this year, the number of the abstracts submitted and those presented crossed the thousand marks. Leading investigators and researchers from all over the world presented the latest developments of their research in the domain of autoimmunity and its correlation with various diseases. In terms of mechanisms of autoimmunity, an update on the mechanisms behind the association of autoimmunity with systemic diseases focusing on hyperstimulation was presented during AUTO12. In addition, a new mechanism of ASIA syndrome caused by an intrauterine contraceptive device was revealed demonstrating a complete resolution of symptoms following device removal. In regard to the correlation between autoimmunity and neurogenerative diseases, the loss of structural protein integrity as the trigger of immunological response was shown. Schizophrenia as well, and its correlation to pro-inflammatory cytokines was also addressed. Furthermore, and as it was said AUTO12 virtual due to COVID-19 pandemic, various works were dedicated to SARS-CoV-2 infection and COVID-19 in terms of autoimmune mechanisms involved in the pathogenesis, treatment and complications of COVID-19. For instance, the correlation between autoimmunity and the severity of COVID-19 was viewed. Moreover, the presence and association of autoantibodies in COVID-19 was also demonstrated, as well as the clinical outcomes of COVID-19 in patients with rheumatic diseases. Finally, immune-mediated reactions and processes secondary to SARS-CoV-2 vaccination was displayed. Due to the immense importance of all of the topics addressed and while several hundreds of works were presented which cannot be summed up in one paper, we aimed hereby to highlight some of the outstanding abstracts and presentations during AUTO12.
Introduction Autoimmunity has served for decades as the connecting base for etiologic and pathogenetic processes of numerous systemic diseases [[1], [2], [3]]. Serving as the first line of defense against invasion, various triggers have been described to dysregulate the immune response causing autoimmune diseases [4]. The triggers of such dysregulated response were shown to be foreign bodies [5], infectious agents [6], chemical or pollution triggers [7] among others. The large base of the connection between autoimmunity and clinical diseases raised the need for a concise gathering of leading experts in the domain of autoimmunity and its branches of clinical immunology, allergy, and rheumatic diseases. Therefore, prof. Shoenfeld was the initiator and leader of organizing an annual meeting under the title of “international congress of autoimmunity” abbreviated as “AUTO” more than a decade ago. The need for such gathering was even greater during the pandemic of COVID-19 since SARS-CoV-2 infection was associated with many immune and autoimmune mechanisms contributing both for morbidity and mortality [8,9], in addition to the role immune-modulators and immunosuppressants have played in the management of patients with COVID-19, particularly in severe disease [10,11]. However, and due to the restrictions of the COVID-19 pandemic, the 12th international congress of autoimmunity (AUTO12) was held virtual this year. Hundreds of abstracts were submitted both for the oral and poster presentation and approximately 500 abstracts were accepted for the congress in all of its sessions. COVID-19 as mentioned, though restricted the physical gathering, constituted a large part of the discussions during the congress. Leading researchers and physicians from more than 40 countries presented in the plenary, parallel and poster sessions. Seeking to spread the knowledge of this important domain for as many colleagues and researchers as possible, we brought here on the tip of the fork some of the lectures presented during AUTO12. As the presentations reached over 500, only a small part was summed up thus called “a taste for more”. An updated medical literature was cited accordingly.
Section snippets Virtual meeting pros and cons, the example of AUTO12 by Jan Damoiseaux The 12th International Congress on Autoimmunity (AUTO12) was originally scheduled for May 2020, but was, due to the SARS-CoV-2 pandemic, first postponed to November 2020 and then to May 2021. However, in the beginning of 2021, it became apparent that a live event was not an option, neither was further postponement. Therefore, it was decided to organize an on-line event with full attention for scientific sessions, poster exhibitions, as well as sponsors. In the virtual conference centerMechanisms of autoimmunity during AUTO12 Prof. Yehuda Shoenfeld illustrated the mechanisms behind developing autoimmune diseases, starting from hyperstimulation or triggering of the immune system. The mechanisms include genetic predisposition, use of adjuvants such as vaccines, foreign bodies or material as silicone, infections, estrogen, prolactin and checkpoint inhibitors among others. Genetic factors are numerous, for instance polymorphism of HLA-DRB1 was shown to be associated with the development of autoimmune diseases [12].Declaration of Competing Interest None.
Researchers discovered a new pathway for the development of Th17 cells, a type of helper T cell involved in autoimmunity. The finding reveals potential new targets for treating autoimmune diseases. Autoimmune diseases arise when the immune system, which normally protects the body from invading microbes, mistakenly attacks the body’s own tissues. These diseases include type 1 diabetes, psoriasis and multiple sclerosis. The immune system employs many different types of cells to regulate disease. A better understanding of the complex signals between these cells will help researchers design better ways to prevent and treat autoimmune diseases. T cells play a major role in the immune system. They can be divided into 2 categories: cytotoxic, which kill infected cells directly, and helper, which make proteins called cytokines that instruct other cells to make certain molecules, move to a specific location or develop in a particular way. Depending on which cytokines are present as a T cell matures, it can become one of many types of helper T cell, each of which has a distinct role in immunity. A team led by Dr. John O’Shea of NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) set out to investigate the development of Th17 cells. These helper T cells make a cytokine called IL-17 that causes inflammation. While helpful for fighting infections, Th17 cells have also been linked with several autoimmune disorders. Past studies have found that a combination of 3 cytokines—interleukin-1-beta (IL-1-beta), interleukin-6 (IL-6) and transforming growth factor beta (TGF-beta)—drive Th17 cell development. However, TGF-beta also drives the development of other T cells (regulatory T cells) that dampen the inflammatory response and help prevent autoimmunity. To further explore Th17 development, the scientists exposed immature mouse T cells to a variety of cytokines in culture. As reported in the October 21, 2010, issue of Nature, replacing TGF-beta with another cytokine, IL-23, worked just as well. Gene expression analysis found that Th17 cells from TGF-beta cultures had higher levels of an anti-inflammatory cytokine called IL-10. In contrast, Th17 cells developed with IL-23 showed higher levels of IL-18R1 and T-bet—2 molecules known to be involved in the development of experimental autoimmune encephalomyelitis (EAE), a mouse disease that resembles human multiple sclerosis. The researchers next looked at the ability of both sets of Th17 cells to cause autoimmune disease. They transferred the cells into mice engineered to lack mature T cells of their own. Mice that received Th17 cells from IL-23 cultures showed more severe symptoms of EAE. This shows that Th17 cells behave differently depending on which cytokines drove their development, with IL-23 producing Th17 cells that are more likely to cause autoimmune disease. These findings shed light on Th17 development, revealing 2 kinds of Th17 cells with distinct functions. The discovery of IL-23 as a driving force in Th17 development points to potential new targets for therapies against autoimmunity.
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Autoimmune Disease
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