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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.
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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