Elsevier

Journal of Autoimmunity

Volume 95, December 2018, Pages 100-123
Journal of Autoimmunity

Molecular mimicry and autoimmunity

https://doi.org/10.1016/j.jaut.2018.10.012Get rights and content
Under a Creative Commons license
open access

Highlights

  • Molecular mimicry occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells

  • Molecular mimicry could be either a deleterious stimulus for the immune system or may help to induce immune tolerance

  • Host genetics, exposure to microbiota and environmental chemicals influence molecular mimicry

  • Autoreactive T cells play a paramount role in molecular mimicry

Abstract

Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual. However, molecular mimicry is unlikely to be the only underlying mechanism for autoimmune responses; other factors such as breach in central tolerance, non-specific bystander activation, or persistent antigenic stimuli (amongst others) may also contribute to the development of autoimmune diseases. Host genetics, exposure to microbiota and environmental chemicals are additional links to our understanding of molecular mimicry. Our current knowledge of the detailed mechanisms of molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease, the lack of enough statistical power in epidemiological studies, the limitations of the potential role of genetics in human studies, the relevance of inbred murine models to the diverse human population and especially the limited technology to systematically dissect the human T-cell repertoire and B-cell responses. Nevertheless, studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of the T-cell receptor repertoires of auto-reactive T-cells, the role of exposure to cryptic antigens, the generation of autoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immune systems all provide clues in advancing our understanding of the molecular mechanisms involved in the evolving concept of molecular mimicry and also may potentially aid in the prevention and treatment of autoimmune diseases.

Keywords

Autoimmune diseases
Autoimmunity
Molecular mimicry
Cross-reactivity
Cross reactions

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