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Infection and Immunity, March 2009, p. 970-976, Vol. 77, No. 3
0019-9567/09/$08.00+0 doi:10.1128/IAI.00833-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Henrik Lambert,1,2,
Polya P. Vutova,1,2
Isabel Dellacasa-Lindberg,1,2
Joanna Nederby,2
Hideo Yagita,3
Hans-Gustaf Ljunggren,1
Alf Grandien,1
Antonio Barragan,1,2* and
Benedict J. Chambers1*
Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden,1 Department of Parasitology, Mycology and Environmental Microbiology, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden,2 Juntendo University School of Medicine, Tokyo 113-8421, Japan3
Received 7 July 2008/ Returned for modification 18 August 2008/ Accepted 1 January 2009
The obligate intracellular parasite Toxoplasma gondii can actively infect any nucleated cell type, including cells from the immune system. In the present study, we observed that a large number of natural killer (NK) cells were infected by T. gondii early after intraperitoneal inoculation of parasites into C57BL/6 mice. Interestingly, one mechanism of NK cell infection involved NK cell-mediated targeting of infected dendritic cells (DC). Perforin-dependent killing of infected DC led to active egress of infectious parasites that rapidly infected adjacent effector NK cells. Infected NK cells were not efficiently targeted by other NK cells. These results suggest that rapid transfer of T. gondii from infected DC to effector NK cells may contribute to the parasite's sequestration and shielding from immune recognition shortly after infection.
Published ahead of print on 12 January 2009.
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