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Infection and Immunity, May 2007, p. 2511-2522, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01818-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Primary Infection of C57BL/6 Mice with Plasmodium yoelii Induces a Heterogeneous Response of NKT Cells

Unité d'Immunophysiopathologie Infectieuse, CNRS URA 1961, Université Paris VI, Institut Pasteur, Paris, France,¹ Département d'Immunologie, Institut Cochin, INSERM U567,² CNRS UMR 8104,³ Hôpital Cochin,⁴ Université René Descartes, Paris, France; CNRS UMR 8147, Université Paris V, Hôpital Necker, Paris, France,⁵ INSERM U511, CHU La Pitié-Salpêtrière, Université Paris VI, Paris, France⁶

Received 15 November 2006/ Returned for modification 14 January 2007/ Accepted 10 February 2007

NKT cells are a population of innate-like lymphocytes that display effector functions and immunoregulatory properties. We characterized the NKT cell response induced in C57BL/6 mice during a primary infection with Plasmodium yoelii sporozoites. We observed a heterogeneous NKT cell response that differed between liver and spleen. Hepatic NKT cells found in infected livers consisted mainly of CD1d-dependent CD4⁺ and double-negative (DN) NKT cells, whereas CD1d-independent NKT cells exhibiting a TCR^high CD4^high phenotype were prominent among splenic NKT cells during the infection. Hepatic and splenic NKT cells isolated from infected mice were activated and secreted mainly gamma interferon and tumor necrosis factor alpha in response to stimulation. Finally, P. yoelii-activated hepatic DN NKT cells inhibited the parasite's liver stage in a CD1d-dependent manner in vitro. However, experiments using B6.CD1d-deficient mice showed that CD1d and CD1d-restricted NKT cells are not necessary to control the parasite's development in vivo during neither the preerythrocytic stage nor the erythrocytic stage. Thus, our results show that a primary P. yoelii infection induces a heterogeneous and organ-specific response of NKT cells and that CD1d-dependent NKT cells play a minor role in the control of the development of Plasmodium in vivo in our model.

Published ahead of print on 16 February 2007.

Editor: W. A. Petri, Jr.

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