title: Gamma delta T cells function in cell-mediated immunity to acute blood-stage Plasmodium chabaudi adami malaria.
abstract: To determine whether gamma delta T cells are essential for the resolution of acute Plasmodium chabaudi adami (P. c. adami) malaria, we depleted gamma delta T cells from C57BL/6 mice with hamster monoclonal anti-TCR gamma delta Ab treatment. During the period in which control mice that had received normal hamster IgG completely resolved infections, gamma delta T cell-depleted mice were unable to suppress their infections. Because the number of splenic CD4+ alpha beta T cells in these anti-TCR-gamma delta-treated mice with nonresolving malaria was similar to control mice, it appears that CD4+ alpha beta T cells alone cannot mediate early resolution even though they are known to play a critical role in immunity to blood-stage malaria. Mice treated with anti-CD4 mAb also failed to resolve P. c. adami malaria. Depletion of CD4+ alpha beta T cells from the spleens of infected mice resulted in minimal expansion of the splenic CD4- gamma delta T cell subset compared with infected control mice. Together, these findings indicate that activation of the gamma delta T cell subset, which requires the presence of CD4+ alpha beta T cells, is essential for resolution of acute P. c. adami malaria. To determine whether gamma delta T cells require either Abs or B cells to achieve their protective activity, B cell-deficient JHD mice were treated with the same depleting anti-TCR-gamma delta Abs. Whereas control JHD mice injected with hamster IgG resolved acute P. c. adami malaria, JHD mice depleted of gamma delta T cells failed to do so. We conclude that gamma delta T cells suppress P. c. adami parasitemia by mechanisms of immunity independent of Ab and B cells.
authors.affiliation: Department of Medical Microbiology and Immunology, University of Wisconsin, Madison 53706, USA.
authors.forename: H C
authors.initials: HC
authors.lastname: van der Heyde
authors.forename: M M
authors.initials: MM
authors.lastname: Elloso
authors.forename: W L
authors.initials: WL
authors.lastname: Chang
authors.forename: M
authors.initials: M
authors.lastname: Kaplan
authors.forename: D D
authors.initials: DD
authors.lastname: Manning
authors.forename: W P
authors.initials: WP
authors.lastname: Weidanz
mesh_terms: D000208:Acute Disease; D000818:Animals; D000913:Antibodies, Protozoan / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D007111:Immunity, Cellular; D008212:Lymphocyte Depletion; D008288:Malaria / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016788:Plasmodium chabaudi / Q000276:immunology*; D010967:Plasmodium yoelii / Q000276:immunology; D016693:Receptors, Antigen, T-Cell, alpha-beta; D016692:Receptors, Antigen, T-Cell, gamma-delta; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D000913:Antibodies, Protozoan; D016693:Receptors, Antigen, T-Cell, alpha-beta; D016692:Receptors, Antigen, T-Cell, gamma-delta