Bisphenol A as a Factor in the Mosaic of Autoimmunity

Author(s):  
Zora Lazurova ◽  
Ivica Lazurova ◽  
Yehuda Shoenfeld

The population worldwide is largely exposed to bisphenol A (BPA), a commonly used plasticizer, that has a similar molecular structure to endogenous estrogens. Therefore, it is able to influence physiological processes in human body, taking part in the pathophysiology of various endocrinopathies, as well as, cardiovascular, neurological and oncological diseases. BPA has been found to affect the immune system, leading to the development of autoimmunity and allergies, too. In the last few decades, the prevalence of autoimmune diseases has significantly increased, that could be explained by a rising exposure of the population to environmental factors, such as BPA. BPA has been found to play a role in the pathogenesis of systemic autoimmune diseases and also organ-specific autoimmunity (thyroid autoimmunity, diabetes mellitus type 1, myocarditis, inflammatory bowel disease, multiple sclerosis, encephalomyelitis etc), but the results of some studies remain still controversial, so further research is needed.

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 91 ◽  
Author(s):  
Elena Gianchecchi ◽  
Alessandra Fierabracci

In recent years, the interest in natural compounds exerting immunoregulatory effects has enormously increased. Among these, the polyphenol resveratrol, found in a variety of foods and beverages, including red grapes and red wine, has been demonstrated to exert both in vitro and in vivo biological activities. More specifically, it has antiaging, cardioprotective, antioxidant, immunomodulatory, anti-inflammatory and chemopreventive activities. Due to its anti-proliferative, pro-apoptotic and immunoregulatory effects, resveratrol has gained substantial attention for the treatment of cancer or autoimmunity, which represent frequently diagnosed diseases with important consequences for the health of the patients affected. The aim of the present review is to focus on the role of resveratrol in the modulation of cancer as well as of several organ-specific or systemic autoimmune diseases, including autoimmune hepatitis, type 1 diabetes mellitus, inflammatory bowel disease, rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis.


1990 ◽  
Vol 172 (2) ◽  
pp. 537-545 ◽  
Author(s):  
S Sakaguchi ◽  
N Sakaguchi

BALB/c athymic nu/nu mice spontaneously developed organ-specific (gastritis, thyroiditis, oophoritis, or orchitis) and systemic (arteritis, glomerulonephritis, and polyarthritis) autoimmune diseases when transplanted with neonatal BALB/c thymuses. Transplantation of thymuses from adult BALB/c mice was far less effective in inducing histologically evident organ-specific autoimmune disease in nu/nu mice. Autoimmune disease developed, however, when adult thymuses were irradiated at a T cell-depleting dose before transplantation. Engrafting newborn thymuses into BALB/c mice T cell depleted by thymectomy, irradiation, and bone marrow transplantation produced similar organ-specific autoimmune disease as well, but thymus engrafting into T cell-nondepleted BALB/c mice (i.e., mice thymectomized as adults, but not irradiated) did not, despite the fact that transplanted thymuses grew well in both groups of mice. The mice with organ-specific autoimmune disease produced autoantibodies specific for the respective organ components, such as gastric parietal cells, thyroglobulins, oocytes, or sperm. The thymus-transplanted nu/nu mice also had hypergammaglobulinemia and developed anti-DNA autoantibodies, rheumatoid factors, and immune complexes in the circulation. These results indicate that: (a) the thymus of a murine strain that does not develop spontaneous autoimmune disease can produce pathogenic self-reactive T cells that mediate organ-specific and/or systemic autoimmune diseases; and (b) such self-reactive T cells, especially those mediating organ-specific autoimmune disease, spontaneously expand and cause autoimmune disease when released to the T cell-deficient or -eliminated periphery.


2009 ◽  
Vol 05 (0) ◽  
pp. 24
Author(s):  
Vincent Geenen ◽  
Olivier Dardenne ◽  
◽  

The discovery that thymic epithelium from many species expresses a large repertoire of genes encoding neuroendocrine and other tissuerestricted antigens has radically changed our knowledge of the pathogenic mechanisms underlying the development of organ-specific autoimmune diseases such as type 1 diabetes and autoimmune endocrine diseases. Rather than a breakdown of immunological selftolerance in periphery, there is mounting evidence that the diabetogenic autoimmune response may first arise from a thymus dysfunction in the central programming of β-cell self-tolerance. Insulin-like growth factor 2 (IGF-2) is the dominant member of the insulin gene/protein family expressed in thymic epithelial cells (TECs) from different species, and Igf2-/- mice fail to programme complete tolerance to insulin. Based on the homology between insulin, the primary and immunogenic auto-antigen of type 1 diabetes, and IGF-2, the tolerogenic selfantigen of the insulin family, the design of a regulatory/negative self-vaccination for prevention against type 1 diabetes has been proposed and is under development.


2021 ◽  
Vol 21 ◽  
Author(s):  
Rakesh K. Sindhu ◽  
Piyush Madaan ◽  
Parteek Chandel ◽  
Rokeya Akter ◽  
G. Adilakshmi ◽  
...  

Background: Autoimmune diseases are the diseases that result due to the overactive immune response, and comprise systemic autoimmune diseases like rheumatoid arthritis (RA), sjӧgren’s syndrome (SS), and organ-specific autoimmune diseases like type-1 diabetes mellitus (T1DM), myasthenia gravis (MG), and inflammatory bowel disease (IBD). Currently, there is no long-term cure; but, several treatments exist which retard the evolution of the disease, embracing gene therapy, which has been scrutinized to hold immense aptitude for the management of autoimmune diseases. Objective: The review highlights the pathogenic mechanisms and genes liable for the development of autoimmune diseases, namely T1DM, type-2 diabetes mellitus (T2DM), RA, SS, IBD, and MG. Furthermore, the review focuses on investigating the outcomes of delivering the corrective genes with their specific viral vectors in various animal models experiencing these diseases to determine the effectiveness of gene therapy. Methods: Numerous review and research articles emphasizing the tremendous potential of gene therapy in the management of autoimmune diseases were procured from PubMed, MEDLINE, Frontier, and other databases and thoroughly studied for writing this review article. Results: The various animal models that experienced treatment with gene therapy have displayed regulation in the levels of proinflammatory cytokines, infiltration of lymphocytes, manifestations associated with autoimmune diseases, and maintained equilibrium in the immune response, thereby hinder the progression of autoimmune diseases. Conclusion: Gene therapy has revealed prodigious aptitude in the management of autoimmune diseases in various animal studies, but further investigation is essential to combat the limitations associated with it and before employing it on humans.


Author(s):  
Laura Räisänen ◽  
Heli Viljakainen ◽  
Catharina Sarkkola ◽  
Kaija-Leena Kolho

AbstractType 1 diabetes mellitus (DM), autoimmune thyroiditis (AIT), juvenile idiopathic arthritis (JIA), and inflammatory bowel diseases (IBD) are common pediatric autoimmune diseases with unknown risk factors. Using nationwide registers, we searched for their perinatal risk factors. Our study followed up 11,407 children (born 2000–2005) for a median of 16.6 years (from birth to 2018). Of them, 2.15% received primary diagnosis and 0.08% also secondary: 0.89% had DM, 0.60% had AIT, 0.48% had JIA, and 0.25% had IBD. The incidences per 100,000 children/year were 106.1 for DM, 46.0 for AIT, 55.0 for JIA, and 23.7 for IBD. There were more preterm births (< 37 weeks) among children with studied autoimmune diseases compared with the rest of the cohort (8.6% vs. 5.3%, p = 0.035). Among those born preterm, children with studied autoimmune diseases received more postnatal antibiotics compared with other preterm children in the cohort (47.6% vs. 27.7%, p = 0.046). Children with IBD were born to older mothers compared with those without studied diagnoses (33.0 vs 30.2, p = 0.004).Conclusion: Preterm birth was a shared risk factor for autoimmune diseases in our study, especially when combined with postnatal antibiotic treatments. High maternal age was associated with IBD. What is Known:• Type 1 diabetes (DM), autoimmune thyroiditis (AIT), juvenile idiopathic arthritis (JIA), and inflammatory bowel diseases (IBD) are common pediatric autoimmune diseases• It is unclear whether these diseases have shared risk factors, since there are no previous simultaneous epidemiological nor follow-up studies on them in one cohort  What is New:• Preterm births were more common in children with DM, AIT, JIA, or IBD compared with other children in the cohort, and preterm children who developed these diseases recieved more postnatal antibiotics compared with other preterm children• High maternal age was associated with IBD


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