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The field of medical research has been always full of innovation and huge leaps revolutionizing the scientific world. In the recent years, we have witnessed this firsthand by the evolution of Artificial Intelligence (AI), with ChatGPT being the most recent example. ChatGPT is a language chat bot which generates human-like texts based on data from the internet. If viewed from a medical point view, ChatGPT has shown capabilities of composing medical texts similar to those depicted by experienced authors, to solve clinical cases, to provide medical solutions, among other fascinating performances. Nevertheless, the value of the results, limitations, and clinical implications still need to be carefully evaluated. In our current paper on the role of ChatGPT in clinical medicine, particularly in the field of autoimmunity, we aimed to illustrate the implication of this technology alongside the latest utilization and limitations. In addition, we included an expert opinion on the cyber-related aspects of the bot potentially contributing to the risks attributed to its use, alongside proposed defense mechanisms. All of that, while taking into consideration the rapidity of the continuous improvement AI experiences on a daily basis. [ABSTRACT FROM AUTHOR]

Abstract Stress is defined as the pscyophysiological reaction in which the steady state is disturbed or threatened. Stress is not always perceived as a negative response. Stress results when environmental demands exceed an individuals' adaptive capacities. Autoimmune diseases are heterogeneous group of chronic diseases which occur secondary to loss of self antigen tolerance. The etiopathogenesis of autoimmune disease is uncertain. Genetic factors as well as environmental factors appear to interplay, leading to a cascade of events resulting in disease onset. Stress has been postulated to play a role in disease onset in the genetically susceptible patients. During the stress response, catecholamines and glucocorticoids are released from locus coeruleus and adrenal gland. These biomolecules exert control over various immune cells in the innate and adaptive arms of the immune system, thereby altering the cytokine profile released. The increase of IL-4 promotes T-helper 2 (T h 2) cell differentiation, while the decrease in IL-12 and the increased IL-10 production reduce the number of T-helper 1 (T h 1) cells. The relationship between stress and autoimmune diseases is intricate. Stress has been shown to be associated with disease onset, and disease exacerbations in rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, Graves' disease as well as other autoimmune conditions. In certain conditions such as psoriasis, stress has been implicated in delaying lesion clearance upon the application of standard treatment regimes. Finally, psychological therapy and cognitive behavioral therapy aimed to reduce stress levels was shown to be effective in influencing better outcomes in many autoimmune diseases. The purpose of this paper is to closer inspect the clinical evidence regarding the role of stress on influencing the various aspects of disease entities. [ABSTRACT FROM AUTHOR]

Polymyalgia rheumatica (PMR) is an inflammatory rheumatic disease that is common in elderly people. Its classification in the spectrum of autoinflammatory and autoimmune diseases is difficult because of its only partially understood immune-mediated mechanisms. The literature concerning the innate and adaptive immune system activation in PMR was systematically reviewed highlighting the relative weight of autoinflammation and autoimmunity in its pathogenesis and disease progression. A literature search on PubMed Central and Embase scientific databases was performed by two independent reviewers. To be eligible, the studies needed to fully satisfy our initial PICO framework: a primary diagnosis of PMR as a population, the search for immune/inflammatory cells, cytokines and autoantibodies as an intervention, a control group consisting in healthy controls, patients with other inflammatory rheumatic diseases or PMR patients in remission after treatment and as outcomes the results of the investigations in the analyzed tissue samples. The most relevant data of the included papers were extracted by using a standardized template. Of the 933 screened abstracts, 52 papers were included in the systematic review and categorized depending on their primary research objectives. The hyper-activity of neutrophils and monocytes, expressing toll-like receptor 7 in active disease, an impaired phagocytosis and endothelial dysfunction, as well as an increased count of innate T cells in patients with remission emerged among the major derangements of the innate immune response in PMR. Among the cytokines profile, interleukin-6 plays a key role but other pro-inflammatory mediators and angiogenesis markers such as chemokines, B-cell activating factor, vascular endothelial growth factor and angiopoietins seem to be involved in refractory or glucocorticoid-resistant PMR. The aberrant adaptive immune response was documented by tissue and serum findings of polarized T cells towards T helper 1 and 17 phenotypes, an increased expression of immunosenescent surface markers and a downregulated immunoregulatory response. The altered distribution of peripheral B cells, detected during active disease, suggested their peripheral migration towards unidentified sites. The interaction between innate and adaptive immune response was documented by a synovial infiltrate of macrophages and T cells. Despite multiple autoantibodies have been detected in PMR patients, none proved to correlate with disease activity seeming to be reactive to the marked inflammation or antigenic determinants provided by environmental triggers or tissue/cell damage. The complex network between innate and adaptive immune system in PMR is supported by findings at molecular and cellular levels. By considering both the ends of the pathophysiological spectrum of immune-mediated rheumatic diseases, PMR may be regarded as an inflammatory immune-mediated disease with mixed mechanisms in a background of genetic and epigenetic factors together with immunological and endocrine senescence. • High concentrations of serum pro-inflammatory cytokines and cell growth factors identify active PMR patients • Innate immune cells might play a role both in PMR disease activity and sub-clinical ongoing inflammation. • T cells are dysregulated in PMR for a hyper-expression of immunosenescent markers and deficient immunoregulatory pathways. • B cells peripheral distribution is altered during active disease suggesting an inflammatory-driven compartmentalization. • Autoantibodies do not seem pathogenetic in PMR but may be reactive to external triggers or damaged tissues self-antigens. [ABSTRACT FROM AUTHOR]

At the 12th International Workshop on Autoantibodies and Autoimmunity (IWAA), organized in August 2014 in Sao Paulo, Brazil, more than 300 autoimmunologists gathered to discuss the status of many novel autoantibodies in clinical practice, and to envisage additional value of autoantibodies in terms of prediction, prognosis and prevention of autoimmune diseases. Two separate workshops were dedicated to standardization and harmonization of autoantibody testing and nomenclature: International Autoantibody Standardization (IAS) and International Consensus on ANA Patterns (ICAP). It was apparent to all in attendance that the discovery and elucidation of novel autoantibodies did not slow down, but that multiple challenges lay ahead of us in order to apply these discoveries to effective and efficient clinical practice. Importantly, this requires optimal bidirectional communication between clinicians and laboratory specialists, as well as close collaboration with the diagnostic industry. This paper is a report on the 12th IWAA in combination with a review of the recent developments in the field of autoantibodies. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To evaluate whether vitamin D levels are related to the risk of developing autoimmune diseases and whether supplementation with vitamin D can modify the course of the diseases. Methods: We reviewed the most relevant papers published from January 1973 to October 2011, using Medline and EMBASE and the search terms “vitamin D”; “autoimmune disease”; “autoimmunity”; “rheumatoid arthritis”; “systemic lupus erythematosus”; “scleroderma”; “systemic sclerosis”; “type 1 diabetes”; “multiple sclerosis”; and “undifferentiated connective tissue disease”. We selected studies on the environmental, genetic and epidemiologic association of vitamin D with autoimmune diseases. Using the strategy described, we identified 1268 articles. 331 articles were eliminated on the basis of the title and another 703 on the basis of the abstract, since they were considered irrelevant for the purposes of the study. Full-text examination was performed on the remaining 234 studies, and a further 15 studies were excluded from the review, since the results had been confirmed or superseded by more recent research. Finally, a systematic review was conducted on 219 articles concerning cross-sectional data on: vitamin D levels and autoimmune diseases; interventional data on vitamin D supplementation in autoimmune diseases; prospective data linking vitamin D level or intake to autoimmune disease risk. Results: Physiopathology studies confirm that hypovitaminosis D, in genetically predisposed subjects, can impair self tolerance by compromising the regulation of dendritic cells, of regulatory T-lymphocytes and of Th1 cells. Cross-sectional studies show that levels of vitamin D <30ng/mL are present in a significant percentage, not only in patients with autoimmune disease, but also in healthy subjects (30–77%), and link profound deficiency (<10ng/mL) with aggravation of symptomatology, while genetic studies associate polymorphism of vitamin D receptors to various autoimmune diseases. Among experimental studies on humans, only those on type-1 diabetes prove that the risks are significantly reduced in infants treated with vitamin D after the 7th month (OR 0.71, 95% CI, 0.60 to 0.84) and that a dose–response effect exists. Conclusions: Basic, genetic, and epidemiological studies indicate a potential role of vitamin D in the prevention of autoimmune diseases, but randomized and controlled trials are necessary to establish the clinical efficacy of vitamin D supplementation in ill or at-risk subjects. [Copyright &y& Elsevier]

Abstract: Endometriosis is a benign gynecologic disorder that affects 5–10% of women of reproductive age worldwide. It is characterized by the presence of ectopic endometrial cells and stroma in various locations outside the endometrium. In some of these women there are also a chronic local inflammatory process and presence of autoantibodies. It is not known whether this process is part of the etiology or is a secondary response to the ectopic cells. Furthermore, endometriosis shares similarities with several autoimmune diseases, which include elevated levels of cytokines, decreased apoptosis, and cell-mediated abnormalities. Our aim in this paper was to review the association between autoimmunity and endometriosis. For this purpose we conducted a thorough literature review in the MEDLINE/PubMed database using the keyword endometriosis crossed with: autoimmune disease, autoimmune diseases, autoimmunity, autoantibodies, immunity, immune-modulation, endometrial antibodies, etc. [Copyright &y& Elsevier]

Abstract: Air pollution consists of a heterogeneous mixture of gasses and particles that include carbon monoxide, nitrates, sulfur dioxide, ozone, lead, toxic by-product of tobacco smoke and particulate matter. Oxidative stress and inflammation induced by inhaled pollutants may result in acute and chronic disorders in the respiratory system, as well as contribute to a state of systemic inflammation and autoimmunity. This paper reviews the mechanisms of air contaminants influencing the immune response and autoimmunity, and it focuses on studies of inhaled pollutants triggering and/or exacerbating rheumatic diseases in cities around the world. Remarkably, environmental factors contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica in rheumatoid arthritis and systemic lupus erythematosus. Other diseases such as scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica. Likewise, primary vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA) may be triggered by silica exposure. Only few studies showed that air pollutants could trigger or exacerbate juvenile idiopathic arthritis and systemic lupus erythematosus. In contrast, no studies of tropospheric pollution triggering inflammatory myopathies and spondyloarthropathies were carried out. In conclusion, air pollution is one of the environmental factors involved in systemic inflammation and autoimmunity. Further studies are needed in order to evaluate air pollutants and their potentially serious effects on autoimmune rheumatic diseases and the mechanisms involved in the onset and the exacerbation of these diseases. [Copyright &y& Elsevier]

Abstract: The past 12 months have witnessed several critical advancements and new particularly promising lines of evidence on the pathogenesis and clinical management of autoimmune diseases. The aim of the present article is to briefly review such progress in specific conditions as well as in autoimmunity in general by highlighting papers published in the Journal of Autoimmunity and in Autoimmunity Reviews. These data cumulatively support the hypothesis that autoimmunity is multifactorial but that specific diseases cluster together; they also continue to reflect the critical relationships between genetics and environmental triggers. [Copyright &y& Elsevier]

Abstract: Pathogenesis of viral origin has long been suggested in autoimmune rheumatic diseases. Beside the well-defined virus induced transient or chronic rheumatic diseases often resembling systemic autoimmune disorders such as rheumatoid arthritis, viruses can contribute to disease pathogenesis by several different pathomechanisms. TT virus is a recently discovered virus of extremely high genetic diversity which commonly infects humans. Despite accumulated evidence on the biological characteristics of TTV, its pathogenicity is still in question; many consider TTV as a harmless endosymbiont. The recent paper overviews the biology of TT virus and investigates the hypothesis that TTV might have a causative role in human diseases with special attention to the possibility that TTV might trigger autoimmunity in rheumatic disorders. [Copyright &y& Elsevier]

Abstract: Among the numerous consequences of globalization, the dissemination of scientific research allows real-time comparisons of clinical and basic experimental data between different geographical areas. As a result, the field of geoepidemiology is now vigorously supported by multiple lines of evidence. This special issue of Autoimmunity Reviews is dedicated to the 2010 International Congress on Autoimmunity and aims to provide a state-of-the-art representation of what is currently known in the field of geoepidemiology for autoimmune diseases. The obvious implications of these observations is a role for environmental factors. We will herein review selected publications from prominent scientific journals to provide the bases to understand some of the lines of evidence proposed in the subsequent papers of this comprehensive volume. The ultimate goal is thus to define whether geoepidemiology should be considered a new challenge for autoimmunologists. [Copyright &y& Elsevier]