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Infection and Immunity, August 2008, p. 3628-3631, Vol. 76, No. 8
0019-9567/08/$08.00+0     doi:10.1128/IAI.00471-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Effector CD8⁺ T Lymphocytes against Liver Stages of Plasmodium yoelii Do Not Require Gamma Interferon for Antiparasite Activity

Sumana Chakravarty, G. Christian Baldeviano, Michael G. Overstreet, and Fidel Zavala^*

Department of Molecular Microbiology and Immunology, Malaria Research Institute, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe Street, Baltimore, Maryland 21205

Received 15 April 2008/ Returned for modification 14 May 2008/ Accepted 22 May 2008

The protective immune response against liver stages of the malaria parasite critically requires CD8⁺ T cells. Although the nature of the effector mechanism utilized by these cells to repress parasite development remains unclear, a critical role for gamma interferon (IFN-) has been widely assumed based on circumstantial evidence. However, the requirement for CD8⁺ T-cell-mediated IFN- production in protective immunity to this pathogen has not been directly tested. In this report, we use an adoptive transfer strategy with circumsporozoite (CS) protein-specific transgenic T cells to examine the role of CD8⁺ T-cell-derived IFN- production in Plasmodium yoelii-infected mice. We show that despite a marginal reduction in the expansion of naive IFN--deficient CS-specific transgenic T cells, their antiparasite activity remains intact. Further, adoptively transferred IFN--deficient CD8⁺ T cells were as efficient as their wild-type counterparts in limiting parasite growth in naive mice. Taken together, these studies demonstrate that IFN- secretion by CS-specific CD8⁺ T cells is not essential to protect mice against live sporozoite challenge.

Published ahead of print on 2 June 2008.

Editor: J. L. Flynn

Present address: Sanaria, Inc., 9800 Medical Center Drive, Rockville, MD 20850.