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Plague, caused by Yersinia pestis, is recognized as the most devastating acute infectious disease experienced by human- kind. This notoriety is based upon the high rate of mortality, the rapid onset, and the appalling pathology associated with both the bubonic and pneumonic forms of the infection. Until recently, these extraordinary symptoms prompted investigators to describe the pestilence as a frontal assault upon the host that overwhelms innate mechanisms of defense, inevitably re- sulting in death caused by septic shock (10, 19). It is now established, however, that the invading organisms inhibit the innate immune response, at least during the late stages of infection, thereby avoiding containment within granulomas (9). The first purpose of this review is to present two seemingly exclusive traditions that purport to define the process whereby yersiniae inhibit the generic inflammatory response. An at- tempt is then made to integrate these concepts. Of the 11 species of Yersinia (genus XI of the Enterobacte- riaceae), those pathogenic to humans are Y. pestis and entero- pathogenic Y. pseudotuberculosis and Y. enterocolitica. These three organisms share an approximately 70-kb plasmid, termed pCD in Y. pestis and pYV in the enteropathogenic species, that encodes at least one determinant required for the downregu- lation of inflammation (9, 75). Despite this common feature, the diseases caused by the two enteropathogenic yersiniae are chronic in nature and otherwise markedly distinct from plague (e.g., Y. pseudotuberculosis usually causes a modest mesenteric lymphadenitis in humans, and Y. enterocolitica typically pro- motes limited gastrointestinal disease). It is therefore remark- able that less than 20,000 years has elapsed since Y. pestis evolved from Y. pseudotuberculosis; divergence of the latter from Y. enterocolitica occurred about 1 million years earlier (1). The close relationship between Y. pestis and Y. pseudotubercu- losis provides an excellent system for defining the hereditary events required for the evolution of acute disease. The known significant changes largely reflect lateral acquisition by Y. pestis of genes permitting infection by fleabite followed by dissemi- nation through interstitial spaces and the lymphatics. In addi- tion, the mutational loss by Y. pestis of functions required by enteropathogenic yersiniae for invasion via the small intestine may further contribute to the severity of plague (9, 75). Addi- tional modifications of the Y. pestis genome that minimize inflammation as a mediator of innate immunity will also be addressed in this report.

Interleukin-10 and Inhibition of Innate Immunity to Yersiniae: Roles of Yops and LcrV (V Antigen)