Borrelia Protein Discovered that Signals the Immune System: “Don’t Eat Me”

Image of lightbulb signifying hopeGLOBE NEWSWIRE (05.07.2024) published an announcement by Bay Area Lyme Foundation regarding groundbreaking data posted on bioRxiv on April 30, 2024. Researchers found a new mechanism of immune evasion used by the bacteria that causes Lyme disease, Borrelia burgdorferi (Bb). Investigators report that bacterial pathogens can evade clearance by macrophages through ‘mimicry’ at the mammalian anti-phagocytic signaling axis between CD47 (ligand) and SIRPα (receptor). A protein, P66 (CD47-like protein), was identified on the surface of Borrelia burgdorferi that is necessary and sufficient to bind the macrophage receptor SIRPα.

This is the first research to identify the specific Borrelia protein that acts as a “don’t eat me” signal to the body’s immune system in people with Lyme disease. This helps answer the question of how Borrelia is able to evade and survive the body’s immune system. Clearance of the bacteria is promoted by blocking of p66 (a protein that has previously been implicated in persistent infection) during infection. Genetic deletion of p66 increases phagocytosis by macrophages. 

The findings of this research offers new insight into bacterial persistence in Lyme patients. It also leads toward new research direction for potential treatments of persistent Lyme disease with P66 as a novel therapeutic target. The research was conducted at Stanford University and University of California San Francisco and funded in part by Bay Area Lyme Foundation. The study is currently in preprint and is expected to be published in a peer-review journal in the future.

For More Information: 

Read the GLOBE NEWSWIRE Announcement

Read the bioRxiv Preprint 

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