Faculty Research 1990 - 1999

Resolution of blood-stage malarial infections in CD8+ cell-deficient beta 2-m0/0 mice.

Document Type

Article

Publication Date

1993

Keywords

Animal, Antigens-CD8: an, Immunity-Cellular, Lymphocyte-Depletion, Malaria: im, Mice, Mutagenesis-Insertional, Plasmodium-chabaudi: im, py, Plasmodium-yoelii: im, py, Species-Specificity, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocyte-Subsets: im

First Page

3187

Last Page

3191

JAX Source

J Immunol 1993 Sep 15;151(6):3187-91

Grant

AI12710/AI/NIAID, AI28802/AI/NIAID, AI24544/AI/NIAID

Abstract

We utilized a definitive model of CD8+ T cell deficiency, the beta 2-microglobulin-deficient (beta 2-m0/0) mouse, to determine whether CD8+ T cells are required in the resolution of blood-stage malaria. In a parallel experiment, C57Bl/6 mice treated with anti-CD8 mAb showed significantly higher levels of parasitemia than untreated C57Bl/6 control mice at several points during the infection. This finding suggests some role for CD8+ cells in containing malaria. However, the beta 2-m0/0 mice, which are genetically blocked from expressing MHC class I or class Ib glycoproteins and therefore have < 2.5% of the normal number of CD8+ T cells, nevertheless resolved infections with three virulence variants of murine Plasmodium. The resolution of Plasmodium chabaudi adami, Plasmodium yoelii yoelii 17X, and Plasmodium chabaudi chabaudi AS infections by beta 2-m0/0 mice in the virtual absence of CD8+ cells demonstrates that these cells are not required to suppress murine malaria and that the suppression mechanism is not MHC class I restricted. The similarity of the time-course for resolution of infection in beta 2-m0/0 and intact control mice with all three subspecies of Plasmodium further supports the lack of a requirement for CD8+ T cells in the suppression of malarial parasitemia.

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