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All  Yersinia  species target and bind to phagocytic cells, but uptake and destruction of bacteria are prevented by injection of anti-phagocytic Yop proteins into the host cell. Here we provide evidence that CD8 +  T cells, which canonically eliminate intracellular pathogens, are important for restricting  Yersinia , even though bacteria are primarily found in an extracellular locale during the course of disease. In a model of infection with attenuated  Y. pseudotuberculosis , mice deficient for CD8 +  T cells were more susceptible to infection than immunocompetent mice. Although exposure to attenuated  Y. pseudotuberculosis  generated T H 1-type antibody responses and conferred protection against challenge with fully virulent bacteria, depletion of CD8 +  T cells during challenge severely compromised protective immunity. Strikingly, mice lacking the T cell effector molecule perforin also succumbed to  Y. pseudotuberculosis  infection. Given that the function of perforin is to kill antigen-presenting cells, we reasoned that cell death marks bacteria-associated host cells for internalization by neighboring phagocytes, thus allowing ingestion and clearance of the attached bacteria. Supportive of this model, cytolytic T cell killing of  Y. pseudotuberculosis –associated host cells results in engulfment by neighboring phagocytes of both bacteria and target cells, bypassing anti-phagocytosis. Our findings are consistent with a novel function for cell-mediated immune responses protecting against extracellular pathogens like  Yersinia : perforin and CD8 +  T cells are critical for hosts to overcome the anti-phagocytic action of Yops.

CD8+ T Cells Restrict Yersinia pseudotuberculosis Infection: Bypass of Anti-Phagocytosis by Targeting Antigen-Presenting Cells