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Infection and Immunity, May 2006, p. 2717-2725, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2717-2725.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Splenic T Cells Regulated by CD4⁺ T Cells Are Required To Control Chronic Plasmodium chabaudi Malaria in the B-Cell-Deficient Mouse

Henri C. van der Heyde,¹ Joan M. Batchelder,² Matyas Sandor,³ and William P. Weidanz^2*

La Jolla Bioengineering Institute, La Jolla, California 92037,¹ Departments of Medical Microbiology and Immunology,² Pathology, University of Wisconsin Medical School, Madison, Wisconsin 53706³

Received 21 December 2005/ Returned for modification 25 January 2006/ Accepted 11 February 2006

Little is known about the function and regulation of splenic T cells during chronic Plasmodium chabaudi malaria. The splenic T-cell population continues to expand, reaching levels equal to 4 times the number of splenocytes in an uninfected mouse. Splenic T cells from J_H^–/– mice with chronic malaria expressed V1⁺ or V4⁺ in the same ratio as uninfected controls with V1 cells dominating, but the V2 ratio declined about twofold. T cells from G8 mice specific for the TL antigen increased only 2-fold in number, compared with 10-fold in BALB/c controls, but G8 T cells failed to express the B220 activation marker. Elimination of the parasite by drug treatment caused a slow depletion in the number of splenic , CD4⁺, and CD8⁺ T cells. Following challenge, drug-cured J_H^–/– mice exhibited nearly identical parasitemia time courses as naïve controls. Depletion of either CD4⁺ T cells or T cells from chronically infected J_H^–/– mice by monoclonal antibody treatment resulted in an immediate and significant (P < 0.05) exacerbation of parasitemia coupled with a marked decrease in splenic T-cell numbers. The number of CD4⁺ T cells, in contrast, did not decrease in mice after anti-T-cell receptor treatment. The results indicate that cell-mediated immunity against blood-stage malarial parasites during chronic malaria (i) requires the continued presence of blood-stage parasites to remain functional, (ii) is dependent upon both T cells and CD4⁺ T cells, and (iii) lacks immunological memory.

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* Corresponding author. Mailing address: University of Wisconsin Medical School, Department of Medical Microbiology and Immunology, 1300 University Avenue, Madison, WI 53706. Phone: (608) 262-9027. Fax: (608) 262-8418. E-mail: wweidanz{at}wisc.edu.

Editor: W. A. Petri, Jr.

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Infection and Immunity, May 2006, p. 2717-2725, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2717-2725.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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