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Visiting Molecular Mimicry Once More: Pathogenicity, Virulence, and Autoimmunity
Yuri Chaves Martins1, Arnon Dias Jurberg2,3, Cláudio Tadeu Daniel-Ribeiro4
1Department of Anesthesiology, Saint Louis University School of Medicine, St. Louis, MO 63110, USA.
Abstract:
The concept of molecular mimicry describes situations in which antigen sharing between parasites and hosts could benefit pathogen evasion from host immune responses. However, antigen sharing can generate host responses to parasite-derived self-like peptides, triggering autoimmunity. Since its conception, molecular mimicry and the consequent potential cross-reactivity following infections have been repeatedly described in humans, raising increasing interest among immunologists. Here, we reviewed this concept focusing on the challenge of maintaining host immune tolerance to self-components in parasitic diseases. We focused on the studies that used genomics and bioinformatics to estimate the extent of antigen sharing between proteomes of different organisms. In addition, we comparatively analyzed human and murine proteomes for peptide sharing with proteomes of pathogenic and non-pathogenic organisms. We conclude that, although the amount of antigenic sharing between hosts and both pathogenic and non-pathogenic parasites and bacteria is massive, the degree of this antigen sharing is not related to pathogenicity or virulence. In addition, because the development of autoimmunity in response to infections by microorganisms endowed with cross-reacting antigens is rare, we conclude that molecular mimicry by itself is not a sufficient factor to disrupt intact self-tolerance mechanisms.
Insights
Molecular mimicry involves antigen sharing between parasites and hosts, potentially causing autoimmunity. Despite massive antigen sharing, it rarely triggers autoimmune diseases, indicating intact self-tolerance mechanisms.
Area of Science:
- Immunology
- Parasitology
- Genomics
Background:
- Molecular mimicry explains how antigen sharing between parasites and hosts can lead to pathogen immune evasion.
- This phenomenon can also trigger autoimmunity due to host responses to parasite-derived self-like peptides.
- Understanding molecular mimicry is crucial for maintaining host immune tolerance in parasitic diseases.
Purpose of the Study:
- To review the concept of molecular mimicry and its implications for host immune tolerance.
- To investigate the extent of antigen sharing between hosts and various organisms using genomics and bioinformatics.
- To analyze peptide sharing between human/murine and microbial proteomes.
Main Methods:
- Review of existing literature on molecular mimicry and autoimmunity.
- Genomic and bioinformatics analyses to quantify antigen sharing between proteomes.
- Comparative analysis of human and murine proteomes against pathogenic and non-pathogenic organisms.
Main Results:
- A massive degree of antigen sharing exists between hosts and both pathogenic and non-pathogenic parasites and bacteria.
- The extent of antigen sharing does not correlate with pathogenicity or virulence.
- Autoimmunity development due to molecular mimicry is rare, even with significant antigen sharing.
Conclusions:
- Molecular mimicry alone is insufficient to break established self-tolerance mechanisms.
- Host immune tolerance remains robust despite extensive antigen sharing with microbes.
- Further research is needed to fully elucidate the complex interplay between molecular mimicry, infection, and autoimmunity.
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