Interaction of Yersinia pestis Virulence Factors with IL-1R/TLR Recognition System

The innate immunity is the first line of defense recognizing commensals and pathogenic microorganisms (1 , 2) . Innate immune responses derive from the ability of cells to rapidly combat invading microorganisms without the requirement for an antigen-specific adaptation. These mechanisms have evolved to recognize common microbe-associated molecular patterns and to interfere with conserved replication and survival strategies that support the propagation of microbial invaders. Toll-like receptors (TLRs) perform the recognition functions. Interleukin (IL)-1 and IL-18 receptors also belong to the TLR family. TLRs are critical proteins linking innate and acquired immunity (3) . In the evolutionary process of host–parasite interrelations, pathogenic microorganisms had been armed with virulence factors specifically interacting with TLRs to manage the innate immunity and evade immunological control. Y. pestis , a causative agent of bubonic and pneumonic plague, inherited immunosuppressive antigen LcrV from its evolutionary ancestor Y. pseudotuberculosis (4) and obtained species specific virulence factors—Caf1 and Pla by acquisition of unique plasmids (5 – 9) . Subunit vaccines based on LcrV and Caf1 are being constructed (10 – 16) . A study of the interaction of Y. pestis virulence factors LcrV, Caf1, and Pla with IL-1 receptor (IL-1R)/TLR system is needed to resolve issues concerned with pathogenesis and construct a new generation of anti-plague vaccines.