Abstract

The pathogenesis of the extremely virulent, gram-negative bacterium Yersinia pestis relies on its ability to evade the innate immune response in mammals to facilitate proliferation in the human host. The outer membrane protein Adhesion invasion locus (Ail) is highly expressed on the bacterial cell surface at 37°C and is a major virulence factor of Y. pestis. Ail interacts with numerous human extracellular matrix proteins to regulate many key steps for Y. pestis infection, including cellular adhesion, immune response evasion, and delivery of cytotoxic Yersinia outer proteins.

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