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Infection and Immunity, April 2002, p. 1750-1760, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1750-1760.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Toxoplasma gondii-Infected Human Myeloid Dendritic Cells Induce T-Lymphocyte Dysfunction and Contact-Dependent Apoptosis

Shuang Wei,1,{dagger} Florentina Marches,1 Jozef Borvak,1 Weiping Zou,1,{dagger} Jacqueline Channon,2 Michael White,3 Jay Radke,3 Marie-France Cesbron-Delauw,4 and Tyler J. Curiel5*

Baylor Institute for Immunology Research, Dallas, Texas 75205,1 Université Joseph Fourier, 38041 Grenoble cedex 9, France,4 Department of Medical Microbiology, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire 03756,2 Montana State University Veterinary Molecular Biology, Bozeman, Montana 59717,3 and Tulane University Medical School, New Orleans, Louisiana 701125

Received 29 June 2001/ Returned for modification 27 August 2001/ Accepted 8 January 2002

Dendritic cells ignite adaptive immunity by priming naïve T lymphocytes. Human monocyte-derived dendritic cells (MDDCs) infected with Toxoplasma gondii induce T-lymphocyte gamma interferon production and may thus activate T. gondii-specific immunity. However, we now demonstrate that T. gondii-infected MDDCs are poor at activating T lymphocytes and are unable to induce specific cytotoxic T lymphocytes. On the other hand, MDDCs acquiring nonviable T. gondii antigens directly, or indirectly through captured apoptotic or necrotic cell bodies, induce potent T-lymphocyte activation. T lymphocytes exposed to infected MDDCs are significantly impaired in upregulation of CD69 and CD28, are refractory to activation, and die through contact-dependent apoptosis mediated by an as-yet-unidentified mechanism not requiring Fas, tumor necrosis factor-related apoptosis-inducing ligand, leukocyte function antigen 1, intercellular adhesion molecule 1, tumor necrosis factor alpha, interleukin 10, alpha interferon, gamma interferon, prostaglandins, or reactive nitrogen intermediates. Bystander T lymphocytes that were neither infected nor apoptotic were refractory to activation, suggesting global dysfunction. Immunosuppression and T-lymphocyte unresponsiveness and apoptosis are typical of acute T. gondii infection. Our data suggest that infected dendritic cells contribute to these processes. On the other hand, host cells infected with T. gondii are resistant to multiple inducers of apoptosis. Thus, regulation of host cell and bystander cell apoptosis by viable T. gondii may be significant components of a strategy to evade immunity and enhance intracellular parasite survival.

* Corresponding author. Mailing address: Tulane Medical School, 1403 Tulane Ave., SL78, New Orleans, LA 70112. Phone: (504) 588-5882. Fax: (504) 588-5483. E-mail: tcuriel{at}tulane.edu.

Editor: S. H. E. Kaufmann

{dagger} Present address: Tulane University Medical School, New Orleans, LA 70112.

Infection and Immunity, April 2002, p. 1750-1760, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1750-1760.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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