A conceptual model of the role of infectious agents in autoimmune diseases

Abstract

The correlation between microbes and autoimmunity is well established, but many underlying mechanisms remain obscure. Thus, this paper attempts to elucidate the role of infectious agents (bacteria, viruses, etc.) in autoimmune diseases. To offer a concise framework for many relevant research findings, the following general conceptual model is proposed and discussed: autoimmune diseases arise from alterations in cells, tissues, or organs, caused by infectious agents. These alterations evolve with time, beginning as subtle, often undetectable changes. As the alterations become more severe, they can be identified by the immune system, which may subsequently attack the infected cells. This process allows for new explanations of relationships between triggers of autoimmunity and infectious agents, the time lag between infection and autoimmune response, the progressive nature of autoimmune diseases, and the role of virus persistence. It can also offer a new point of view on molecular mimicry and epitope spreading. The roles of genetic predisposition, sex, stress, dietary habits, the “hygiene hypothesis,” and the healing effects of β-interferon also fit into this framework. In addition, the side effects of malignancy treatments using immune checkpoint inhibitors can also be explained. Adhering to the framework, it is concluded that treatments should aim to eliminate the cause of these evolving alterations, namely, the infectious agents. Presumably, they could be based on antibiotics and antiviral drugs. Future research directions are suggested for evaluating the proposed conceptual model.

Keywords

Autoimmune diseases / Infectious agents / Molecular mimicry / Epitope spreading / Hygiene hypothesis / Virus persistence / Immune checkpoint inhibitors / Resilience

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