A Contribution to the Conceptual Model of Occurrence of Autoimmune Diseases

In this paper, an attempt is made to shed additional light on the role of infectious agents (bacteria, viruses, etc.) in autoimmune diseases. While the correlation between them is well established, many points remain obscure. To offer a concise framework for many of the relevant research findings, the following conceptual model is discussed: autoimmune diseases are due to alterations of cells, tissues or organs, which are caused by infectious agents. These alterations evolve with time. Initially they are small and hardly detectable. As they become more severe, though, they are traced, and the infected cells are subsequently attacked by the immune system. The aforementioned process allows for new explanations of the relationship between triggers of autoimmunity and infectious agents, of the time lag between infection and autoimmune response and of the progressive nature of autoimmune diseases. It can also offer a new point of view of molecular mimicry and of epitope spreading. The roles of genetic predisposition, stress, diet habits and lifestyle fit in its framework, as well. Side effects of malignancy treatments using immune checkpoint inhibitors can also be explained. A conclusion of the aforementioned reasoning is that treatments should aim to completely eliminate the cause of these evolving alterations, namely the infectious agents. Presumably, they could be based on antibiotics and antiviral drugs. Τo check the validity of the proposed conceptual model, research directions are suggested in the last section of the paper.