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Infection and Immunity, January 2002, p. 36-48, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.36-48.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

During Trypanosoma cruzi Infection CD1d-Restricted NK T Cells Limit Parasitemia and Augment the Antibody Response to a Glycophosphoinositol-Modified Surface Protein

Malcolm S. Duthie,1 Monika Wleklinski-Lee,1 Sherilyn Smith,1 Toshinori Nakayama,2 Masaru Taniguchi,2 and Stuart J. Kahn1,3*

Departments of Pediatrics,1 Department of Molecular Immunology, Chiba University, Chiba, Japan,2 Pathobiology, University of Washington, Seattle, Washington 981953

Received 18 May 2001/ Returned for modification 25 July 2001/ Accepted 1 October 2001

Trypanosoma cruzi is a protozoan parasite that chronically infects many mammalian species and in humans causes Chagas’ disease, a chronic inflammatory disease. The parasite expresses glycophosphoinositol (GPI), which potently stimulates interleukin 12 (IL-12) production. During T. cruzi infection IL-12, and possibly GPI, might stimulate NK T cells to affect the protective and chronic inflammatory responses. Here we report that during T. cruzi infection CD1d-restricted NK T cells are stimulated as NK T-cell-deficient mice have greater parasitemia. Furthermore, during T. cruzi infection the percentages of NK T cells in the liver and spleen become decreased for prolonged periods of time, and in vitro stimulation of NK T cells derived from livers of chronically infected mice, compared to uninfected mice, results in increased gamma interferon and IL-4 secretion. Moreover, in NK T-cell-deficient mice the chronic-phase antibody response to a GPI-modified surface protein is decreased. These results indicate that, during the acute infection, NK T cells limit parasitemia and that, during the chronic phase, NK T cells augment the antibody response. Thus, during T. cruzi infection the quality of an individual’s NK T-cell response can affect the level of parasitemia and parasite tissue burden, the intensity of the chronic inflammatory responses, and possibly the outcome of Chagas’ disease.

* Corresponding author. Mailing address: Department of Pediatrics, University of Washington, Box 356320, 1959 N.E. Pacific St., Seattle, WA 98195-6320. Phone: (206) 543-4424. Fax: (206) 221-5469. E-mail: stujk{at}u.washington.edu.

Editor: J. M. Mansfield

Infection and Immunity, January 2002, p. 36-48, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.36-48.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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