[Molecular mimicry between human thyroid peroxidase, thyroglobulin, cosinophil peroxidase, IL-24 and microorganisms...

Area of Science:

• Immunology
• Molecular Biology
• Bioinformatics

Context:

• Autoimmune diseases like urticaria and hypothyroidism are sometimes linked to infections.
• The underlying mechanisms for this association remain unclear.
• Molecular mimicry is a proposed mechanism where microbial antigens resemble self-antigens, potentially triggering autoimmune responses.

Purpose:

• To identify molecular mimicry between human proteins (thyroid peroxidase [TPO], eosinophil peroxidase [EPX], thyroglobulin, IL24) and microbial antigens.
• To investigate potential cross-reactive epitopes shared between human proteins and antigens from parasites and bacteria.

Summary:

• In silico analysis revealed molecular mimicry between TPO/EPX and antigens from bacteria (e.g., Campylobacter jejuni) and nematodes (e.g., Anisakis simplex, Toxocara canis, Trichinella pseudospiralis).
• Specifically, 38 microbial antigens showed 30-45% identity with human proteins, with significant alignments found between Anisakis simplex proteins and EPX.
• 220 epitopes were predicted, with 10 shared epitopes identified between peroxidasin-like proteins and TPO/EPX, suggesting potential cross-reactivity.

Impact:

• These findings suggest molecular mimicry could be a key mechanism linking infections to urticaria and hypothyroidism.
• The study highlights specific microbial antigens and epitopes involved in potential cross-reactivity.
• Further in vitro validation is required to confirm these in silico predictions and elucidate the role of molecular mimicry in these autoimmune conditions.