title: Expansion of the gammadelta T cell subset in vivo during bloodstage malaria in B cell-deficient mice.
abstract: Mice rendered B cell-deficient either by chronic anti-mu treatment initiated at birth or by gene knockout (JHD and mu-MT mice) suppressed acute Plasmodium chabaudi infections with a time course similar to intact control mice. Moreover, both kinds of B cell-deficient mice showed a 50- to 100-fold increase in splenic gammadelta T cell number after suppression of parasitemia compared with uninfected B cell-deficient controls; the magnitude of this increase resulted in significantly (P< 0.05) greater numbers of splenic gammadelta T cells in the B cell-deficient mice than in infected B cell-intact controls (about 10-fold). In contrast, the number of splenic CD4+ alphabeta T cells was only slightly elevated (< 2-fold) in both kinds of B cell-deficient mice compared with their intact controls. The number of splenic gammadelta T cells following suppression of P. vinckei parasitemia was approximately ninefold greater in JHD mice than in C57BL/6 controls, whereas similar numbers of splenic CD4+ alphabeta T cells were detected. Maximal numbers of gammadelta T cells were in cell-cycle in both JHD and C57BL/6 mice during descending P. chabaudi parasitemia, but the number of gammadelta T cells in cell-cycle was greater in B cell-deficient mice than in intact controls. Interleukin-10 (IL-10), a potent TH1 cell-suppressive molecule, does not appear to down-regulate the gammadelta T cell response during malaria in B cell-intact mice because the magnitude of the gammadelta T cell response was not significantly greater in IL-10 knockout mice compared with heterozygote controls. These findings collectively indicate that a markedly enhanced expansion of the gamma delta T cell population occurs in the absence of B cells, and this expansion occurs predominantly during acute malaria when parasite burdens are similar in B cell-deficient animals and intact controls.
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: B J
authors.initials: BJ
authors.lastname: Pepper
authors.forename: J
authors.initials: J
authors.lastname: Batchelder
authors.forename: W P
authors.initials: WP
authors.lastname: Weidanz
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000502:physiology*; D005260:Female; D016753:Interleukin-10 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000502:physiology; D008288:Malaria / Q000097:blood* / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D016788:Plasmodium chabaudi; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000502:physiology*; D016176:T-Lymphocyte Subsets / Q000502:physiology*; D013601:T-Lymphocytes / Q000378:metabolism
chemical_list: D016692:Receptors, Antigen, T-Cell, gamma-delta; D016753:Interleukin-10