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| Psoriasis (a type of auto-immune disease) |
Abstract
Autoimmune diseases, including multiple sclerosis and type 1 diabetes mellitus, affect about 5% of the worldwide population. In the last decade, reports have accumulated on various autoimmune disorders, such as idiopathic thrombocytopenia purpura, myopericarditis, primary ovarian failure, and systemic lupus erythematosus (SLE), following vaccination. In this review, we discuss the possible underlying mechanisms of autoimmune reactions following vaccinations and review cases of autoimmune diseases that have been correlated with vaccination. Molecular mimicry and bystander activation are reported as possible mechanisms by which vaccines can cause autoimmune reactions. The individuals who might be susceptible to develop these reactions could be especially not only those with previous post-vaccination phenomena and those with allergies but also in individuals who are prone to develop autoimmune diseases, such as those with a family history of autoimmunity or with known autoantibodies, and the genetic predisposed individuals.
Further research is encouraged into the direct associations between vaccines and autoimmune conditions, and the biological mechanisms behind them.
Introduction
Although the vaccines are generally safe, with a low incidence of serious systemic adverse events, numerous reports highlighted the occurrence of neurological (Guillain Barre syndrome, multiple sclerosis, autism), articular (arthritis, rheumatoid arthritis), and autoimmune untoward effects (systemic lupus erythematosus, diabetes mellitus) after single or combined multivaccine procedures (Table (Table1)1) [4].
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| Table 1 - Autoimmune diseases reported after vaccination (Source | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607155/) |
In the 1994, Stratton and coworkers published the first report on a causal relationship between several vaccines (e.g., diphtheria, tetanus toxoids, oral polio vaccines) and autoimmune disorders (e.g., Guillain–Barre syndrome, type 1 diabetes, and multiple sclerosis) [5].
These autoimmune disorders (rheumatic, endocrinological, and gastrointestinal diseases) are increased significantly over the last 30 years and affect more than 5% of the individuals worldwide at the age of vaccination programs, which is quite different compared to the spontaneous autoimmune disease incidence [6–9]. These observations raise the problem whether vaccination should be recommended or avoided in autoimmune risk patients [10].
The etiology and the trigger mechanism of autoimmune disease are still unclear [11], but several studies suggest that a vaccine component (inactive viral/bacterial agent or attenuated living microorganism) or a wild superimposed infectious agent can induce autoimmune disease in people with a genetic predisposition [12, 13]. For instance, Borrelia burgdorferi and group A-hemolytic streptococcus contained in the Lyme disease and S. pyogenes vaccines can cause chronic arthritis and rheumatic heart disease, respectively [14, 15].
The autoimmune reaction to specific self-antigens can be tissue-specific (such as thyroid, β-cells of the pancreas), where unique tissue-specific antigens are targeted, or systemic, with multiple tissues affected, and a variety of expressed autoantigens are targeted [2].
The main pathogenic mechanisms of autoimmune disease are the following:
(1) Molecular mimicry by which viral or bacterial agents trigger an immune response against autoantigens: the susceptible host is infected by an agent carrying antigens immunologically similar to the host antigens but trigger a different immune response when presented to T cells. As a result, the tolerance to autoantigens breaks down, and the pathogen-specific immune response causes tissue damage [11, 16];
(2) Bystander activation by which microbial agents release sequestered self-antigens from host tissue that activate antigen-presenting cells (APCs) and dormant autoreactive T-helper cells. These auto-reactive T cells, along with macrophages, secrete cytokines, and an additive effect results in local inflammation and the recruitment of additional T-helper cells.
We searched, Pubmed/Medline between 1980 and 2016, the issue of immune disorders following vaccination in order to review the state of the art and outline the possible pathogenic link (see Table Table11).
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Conclusion
The vaccination might display autoimmune side effects and potentially even trigger a full-blown autoimmune disease. This susceptibility to vaccine-induced autoimmunity is probably determined also by genetic predisposition, which further emphasizes the importance of “the mosaic of autoimmunity” [4]. The vaccination decreases the morbidity and mortality of the individuals, especially children. Nevertheless, the dilemma of whom and when to vaccinate remains unresolved and further research is needed to explain the action mechanism.
Finally, we believe that our commitment should be to plan genetic investigations on the post-vaccination autoimmune-affected patients in order to clarify the pathogenic background and the physiopathology of vaccine-related autoimmune response. Hopefully, this approach might lead to outline a screen-test (patch test?) for this risk and, eventually, to prevention of adverse reactions by vaccination. It could represent a “personalized medicine” that could potentially improve preventive methods and therapeutic options, accordingly with the recommendations of the “European Association for Predictive, Preventive and Personalised Medicine” [166].
( Read the original article in FULL here: Vaccination and autoimmune diseases: is prevention of adverse health effects on the horizon? [Ncbi.nlm.nih.gov]
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