Leah Ragosta

The research I have worked on focuses on how the Lyme disease-causing bacterium Borrelia burgdorferi evades immune clearance through a novel interaction between its surface protein P66 and the mammalian receptor SIRPα. P66 acts as a 'don't eat me' signal, mimicking the human CD47-SIRPα axis to suppress macrophage-mediated phagocytosis. Characterizing this mechanism will give insights into pathogen immune evasion and potential therapeutic targets.

This research investigates the role of the Borrelia burgdorferi surface protein P66 in immune evasion, particularly how it interacts with the mammalian receptor SIRPα to suppress macrophage-mediated phagocytosis. Experiments have demonstrated that P66 functions as a bacterial mimic of CD47, a well-known ‘don’t eat me’ signal, allowing B. burgdorferi to evade immune clearance. Using techniques such as flow cytometry and bacterial pelleting assays, I have characterized the molecular interactions between P66 and SIRPα, identifying key residues essential for binding. Given that SIRPα is highly polymorphic across human populations, this work also raises questions about how genetic variation might influence susceptibility to Lyme disease. By elucidating this immune evasion strategy, this research could inform the development of novel therapeutics that enhance macrophage clearance of B. burgdorferi.