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Are Autoimmune Diseases Caused by Infections?


To address the question of whether autoimmune diseases can be induced by infections, first autoimmunity needs to be defined. Autoimmune disease occurs when a response against a self-antigen(s) involving T cells, B cells, or autoantibodies induces injury systemically or against a particular organ. Understanding of autoimmune diseases is hindered by the fact that some level of autoimmunity, in the form of naturally occurring autoantibodies and self-reactive T and B cells, is present in all normal persons . Thus, on a proportional basis, developing autoimmune disease is the relatively uncommon consequence of a common autoimmune response. Although an autoimmune response occurs in most persons, clinically relevant autoimmune disease develops only in susceptible persons .


Given those circumstances, how can infections induce autoimmune disease? A mechanism often called on to explain the association of infection with autoimmune disease is "molecular mimicry," that is, antigens (or more properly epitopes) of the microorganism closely resemble self-antigens. The induction of an immune response to the microbial antigen thus results in cross-reaction with self-antigens and induction of autoimmunity . Although epitope-specific cross-reactivity between microbes and self-tissues has been shown in some animal models , molecular mimicry has not been clearly demonstrated to occur in human diseases . Another possibility is that microorganisms expose self-antigens to the immune system by directly damaging tissues during an active infection. This mechanism has been referred to as the "bystander effect" . However, whether pathogens mimic self-antigens, release sequestered self-antigens, or both, is difficult to determine.

In addition to antigen-specific mechanisms, nonspecific mechanisms could also lead to autoimmunity after infection .  During mechanical injury, self-antigens and cytokines are released without consistently stimulating pathogen-specific responses. Autoimmune disease rarely develops and usually resolves spontaneously, as seen in postcommissurotomy syndrome (or postcardiotomy syndrome). Adjuvants (usually bacterial, e.g., Mycobacterium in complete Freunds adjuvant) activate the innate immune response in the same pathogen-specific manner when administered with self-antigen; this process results in organ-specific autoimmune disease in animal models . Adjuvant alone (without self-antigen) does not usually result in autoimmune disease, and microorganisms likely provide not only the adjuvant effect to stimulate the immune response but also the damage necessary to make self-antigens available to the immune system, resulting in autoimmune disease.

To determine whether infection can lead to autoimmune disease, direct evidence (e.g., the ability to transfer autoimmune disease), indirect evidence (e.g., the ability to reproduce autoimmune disease in animal models), and circumstantial evidence (e.g., the association of autoantibodies with disease in appropriate clinical settings) should be considered (3,6). The best evidence so far that infections can induce autoimmune diseases comes from animal models. In most animal models of autoimmunity, including myocarditis, disease has been transferred to na´ve animals with autoimmune cells (splenocytes or T cells), autoantibodies (7), or both, which provides compelling evidence that infections induce autoimmune diseases by immune-mediated mechanisms.

Lessons from Coxsackievirus B3 (CB3) Myocarditis.Today Covid is triggering multiple autoimmune diseases like GBS, Myocaditis, Acute inflmmatory syndrome

Genetics of Susceptibility to Myocarditis

Genetic background accounts for only about one third (30%-35%) of the risk of autoimmune disease  This estimate is based on studies that compared genetically identical, monozygotic twins to nonidentical, dizygotic pairs, for which the concurrence rate can be as low as 2% to 7% . Therefore, noninherited factors account for the remaining (approximately 70%) risk of developing an autoimmune disorder. Yet, even identical twins do not have identical immune systems. Genes outside of the MHC contribute to the risk for autoimmune disease. However, little information is available about the function of these non-MHC genes. Recent studies have focused on regulatory signals, and considerable evidence exists that cytotoxic lymphocyte antigen-4 (CTLA-4), which provides a downregulatory signal, influences susceptibility to autoimmunity Genes that involve apoptosis, a common pathway by which immune responses generally are terminated, may also predispose persons to autoimmune disease .

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