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The Journal of Immunology, 2007, 179: 8357-8365.
Copyright © 2007 by The American Association of Immunologists, Inc.
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Death Receptor Ligation or Exposure to Perforin Trigger Rapid Egress of the Intracellular Parasite Toxoplasma gondii1

Emma K. Persson2,*,{ddagger}, Abela Mpobela Agnarson2,*,{ddagger}, Henrik Lambert*,{ddagger}, Niclas Hitziger*,{ddagger}, Hideo Yagita§, Benedict J. Chambers*, Antonio Barragan3,*,{ddagger} and Alf Grandien3,*,{dagger}

* Center for Infectious Medicine and {dagger} Center for Experimental Hematology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital–Huddinge, Stockholm, Sweden; {ddagger} Swedish Institute for Infectious Disease Control, Stockholm, Sweden; and § Department of Immunology, Juntendo University, School of Medicine, Tokyo, Japan

The obligate intracellular parasite Toxoplasma gondii chronically infects up to one-third of the global population, can result in severe disease in immunocompromised individuals, and can be teratogenic. In this study, we demonstrate that death receptor ligation in T. gondii-infected cells leads to rapid egress of infectious parasites and lytic necrosis of the host cell, an active process mediated through the release of intracellular calcium as a consequence of caspase activation early in the apoptotic cascade. Upon acting on infected cells via death receptor- or perforin-dependent pathways, T cells induce rapid egress of infectious parasites able to infect surrounding cells, including the Ag-specific effector cells.

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 work supported by in part by grants from the Swedish Research Council (to A.B.), the Swedish Cancer Society (to A.G.), and the Swedish Foundation for Strategic Research. N.H. is the recipient of a postdoctoral fellowship from the Karolinska Institutet infection network.

2 E.K.P. and A.M.A. contributed equally to this work.

3 Address correspondence and reprint requests to Dr. Alf Grandien or Dr. Antonio Barragan, Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital–Huddinge, 141 86 Stockholm, Sweden. E-mail addresses: Alf.Grandien{at}ki.se and Antonio.Barragan{at}ki.se

4 Abbreviations used in this paper: m, murine (prefix); BMDC, bone marrow-derived dendritic cell; CrmA, cytokine response modifier A; FasL, Fas ligand; h, human (prefix); PI, propidium iodide; wt, wild type; z-VAD-FMK, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone.

5 The online version of this article contains supplemental material.


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The JI 2007 179: 7991-7992. [Full Text]  





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