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Updated: Feb 10, 2026

Molecular Evolution of the Tre Recombinase

Molecular Evolution of the Tre Recombinase

Published on: May 29, 2008

Molecular (Me)micry?

Orly Avni¹, Omry Koren¹

¹Azrieli Faculty of Medicine, Bar Ilan University, Safed, Israel.

Cell Host & Microbe

|May 11, 2018

Summary

This summary is machine-generated.

Molecular mimicry, where microbes resemble human proteins, can trigger autoimmune diseases like lupus. This immune system "friendly fire" occurs when the body mistakenly attacks its own tissues due to microbial similarities.

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Area of Science:

Immunology
Microbiology
Autoimmunity

Background:

Molecular mimicry between the human body and microorganisms is a significant factor in immune system function.
The immune system can be misdirected by microbial components that resemble self-antigens, leading to autoimmune responses.

Purpose of the Study:

To investigate the role of molecular mimicry in the development of autoimmune diseases.
To understand how microbial factors can trigger self-directed immune attacks, using lupus as a model.

Main Methods:

Analysis of molecular mimicry between microbial antigens and human autoantigens.
Investigating the immune response triggered by microbial-Ro60 in the context of lupus.

Main Results:

Demonstrated a common occurrence of molecular mimicry between humans and the microbiota.
Identified microbial-Ro60 as a potential trigger for the autoimmune disease lupus through molecular mimicry.

Conclusions:

Molecular mimicry is a critical mechanism that can mislead the immune system.
Microbial mimicry can result in autoimmune diseases, such as lupus, due to immune system "friendly fire" against host tissues.