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Recognition of Toxoplasma gondii by TLR11 Prevents Parasite-Induced Immunopathology¹

Felix Yarovinsky^2,*,, Sara Hieny and Alan Sher

^* Department of Immunology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390; and Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

TLRs are thought to play a critical role in self/non-self discrimination by sensing microbial infections and initiating both innate and adaptive immunity. In this study, we demonstrate that in the absence of TLR11, a major TLR involved in recognition of Toxoplasma gondii, infection with this protozoan parasite induces an abnormal immunopathological response consisting of pancreatic tissue destruction, fat necrosis, and systemic elevations in inflammatory reactants. We further show that this immunopathology is the result of non-TLR dependent activation of IFN- secretion by NK cells in response to the infection. These findings reveal that in addition to triggering host resistance to infection, TLR recognition can be critical for the prevention of pathogen-induced immune destruction of self tissue.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This project was supported (in part) by the National Institute of Allergy and Infectious Diseases intramural program and by the University of Texas Southwestern Medical Center Endowed Scholars Program.

² Address correspondence and reprint requests to Dr. Felix Yarovinsky, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390. E-mail address: Felix.Yarovinsky{at}UTSouthwestern.edu

³ Abbreviations used in this paper: DC, dendritic cell; WT, wild type; ALT, alanine aminotransferase; AST, aspartate aminotransferase.