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The Journal of Immunology, Vol 149, Issue 1 175-180, Copyright © 1992 by American Association of Immunologists

ARTICLES

Simultaneous depletion of CD4+ and CD8+ T lymphocytes is required to reactivate chronic infection with Toxoplasma gondii

R Gazzinelli, Y Xu, S Hieny, A Cheever and A Sher
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.

C57BL/6 mice chronically infected with an avirulent strain (ME-49) of Toxoplasma gondii were used to study the mechanisms by which T lymphocytes and IFN-gamma prevent reactivation of latent infection. Infected animals were treated with mAb, either anti-CD8, anti-CD4, anti- CD4 plus anti-CD8, anti-IFN-gamma, or anti-CD4 plus anti-IFN-gamma and the mice followed for survival, histopathology, cyst numbers, and spleen cell cytokine responses. In agreement with previously published findings, treatment with anti-IFN-gamma antibodies fully reactivated the asymptomatic infection, inducing massive necrotic areas in the brain with the appearance of free tachyzoites and death of all animals within 2 wk. Mice treated with the combination of anti-CD4 plus anti- CD8 antibodies showed augmented pathology and mortality nearly identical to the anti-IFN-gamma- treated animals. In contrast, treatment with anti-CD4 or anti-CD8 mAb alone failed to result in significantly enhanced brain pathology or mortality. In additional experiments, full reactivation of infection was observed in mice treated with anti-CD4 plus anti-IFN-gamma indicating that CD4+ lymphocytes are not required for the pathology resulting from IFN-gamma neutralization. Cytokine measurements on parasite Ag-stimulated spleen cells from mAb-treated mice indicated that both CD4+ and CD8+ cells produce IFN-gamma whereas only CD4+ cells contribute to parasite Ag- induced IL-2 synthesis. Together, these results suggest that CD4+ and CD8+ lymphocytes act additively or synergistically to prevent reactivation of chronic T. gondii infection probably through the production of IFN-gamma.


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 Infect. Immun.Home page
N. M. Silva, R. T. Gazzinelli, D. A. O. Silva, E. A. V. Ferro, L. H. Kasper, and J. R. Mineo
Expression of Toxoplasma gondii-Specific Heat Shock Protein 70 during In Vivo Conversion of Bradyzoites to Tachyzoites
Infect. Immun., August 1, 1998; 66(8): 3959 - 3963.
[Abstract] [Full Text] [PDF]

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 Clin. Microbiol. Rev.Home page
J. P. Dubey, D. S. Lindsay, and C. A. Speer
Structures of Toxoplasma gondii Tachyzoites, Bradyzoites, and Sporozoites and Biology and Development of Tissue Cysts
Clin. Microbiol. Rev., April 1, 1998; 11(2): 267 - 299.
[Abstract] [Full Text] [PDF]

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 J. Immunol.Home page
C. S. Subauste, F. Fuh, R. de Waal Malefyt, and J. S. Remington
{alpha}{beta} T Cell Response to Toxoplasma gondii in Previously Unexposed Individuals
J. Immunol., April 1, 1998; 160(7): 3403 - 3411.
[Abstract] [Full Text] [PDF]

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 J. Immunol.Home page
M. Deckert-Schluter, H. Bluethmann, A. Rang, H. Hof, and D. Schluter
Crucial Role of TNF Receptor Type 1 (p55), But Not of TNF Receptor Type 2 (p75), in Murine Toxoplasmosis
J. Immunol., April 1, 1998; 160(7): 3427 - 3436.
[Abstract] [Full Text] [PDF]

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 J. Immunol.Home page
G. S. Yap, T. Scharton-Kersten, H. Charest, and A. Sher
Decreased Resistance of TNF Receptor p55- and p75-Deficient Mice to Chronic Toxoplasmosis Despite Normal Activation of Inducible Nitric Oxide Synthase In Vivo
J. Immunol., February 1, 1998; 160(3): 1340 - 1345.
[Abstract] [Full Text] [PDF]

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 JEMHome page
L. L. Johnson and P. C. Sayles
Interleukin-12, Dendritic Cells, and the Initiation of Host-protective Mechanisms against Toxoplasma gondii
J. Exp. Med., December 1, 1997; 186(11): 1799 - 1802.
[Full Text] [PDF]

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 JEMHome page
T. M. Scharton-Kersten, G. Yap, J. Magram, and A. Sher
Inducible Nitric Oxide Is Essential for Host Control of Persistent but Not Acute Infection with the Intracellular Pathogen Toxoplasma gondii
J. Exp. Med., April 7, 1997; 185(7): 1261 - 1274.
[Abstract] [Full Text] [PDF]


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