title: Resistance to malarial infection is achieved by the cooperation of NK1.1(+) and NK1.1(-) subsets of intermediate TCR cells which are constituents of innate immunity.
abstract: We previously reported that the major expanding lymphocytes were intermediate TCR (TCR(int)) cells (mainly NK1.1(-)) during malarial infection in mice. Cell transfer experiments of TCR(int) cells indicated that these T cells mediated resistance to malaria. However, TCR(int) cells always contain NK1.1(+)TCR(int) cells (i.e., NKT cells) and controversial results (NKT cells were effective or not for resistance to malaria) have been reported by different investigators. In this study, we used CD1d((-/-)) mice, which almost completely lack NKT cells in the liver and other immune organs. Parasitemia was prolonged in the blood of CD1d((-/-)) mice and the expansion of lymphocytes in the liver of these mice was more prominent after an injection of Plasmodium yoelii-infected erythrocytes. However, these mice finally recovered from malaria. In contrast to B6 mice, CD4(-)8(-) NKT cells as well as NK1.1(-)CD3(int) cells expanded in CD1d((-/-)) mice after malarial infection, instead of CD4(+) (and CD8(+)) NKT cells. These newly generated CD4(-)8(-)NKT cells in CD1d((-/-)) mice did not use an invariant chain of Valpha14Jalpha281 for TCRalpha. Other evidence was that severe thymic atrophy and autoantibody production were accompanied by malarial infection, irrespective of the mice used. These results suggest that both NK1.1(-) and NK1.1(+) subsets of TCR(int) cells (i.e., constituents of innate immunity) are associated with resistance to malaria and that an autoimmune-like state is induced during malarial infection.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Niigata, 951-8510, Japan.
authors.forename: M K
authors.initials: MK
authors.lastname: Mannoor
authors.forename: A
authors.initials: A
authors.lastname: Weerasinghe
authors.forename: R C
authors.initials: RC
authors.lastname: Halder
authors.forename: S
authors.initials: S
authors.lastname: Reza
authors.forename: M
authors.initials: M
authors.lastname: Morshed
authors.forename: A
authors.initials: A
authors.lastname: Ariyasinghe
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: H
authors.initials: H
authors.lastname: Sekikawa
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology*; D018949:Antigens, CD1 / Q000235:genetics / Q000276:immunology; D055610:Antigens, CD1d; D000944:Antigens, Differentiation, B-Lymphocyte; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex / Q000276:immunology; D004195:Disease Models, Animal; D000949:Histocompatibility Antigens Class II; D007113:Immunity, Innate / Q000276:immunology; D016130:Immunophenotyping; D007371:Interferon-gamma / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D007694:Killer Cells, Natural / Q000276:immunology*; D007700:Kinetics; D037181:Lectins, C-Type; D008099:Liver / Q000293:injuries / Q000473:pathology; D018655:Lymphocyte Count; D008288:Malaria / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008819:Mice, Nude; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010967:Plasmodium yoelii / Q000276:immunology*; D011506:Proteins / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors
chemical_list: D000941:Antigens; D018949:Antigens, CD1; D055610:Antigens, CD1d; D000944:Antigens, Differentiation, B-Lymphocyte; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex; D000949:Histocompatibility Antigens Class II; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D016693:Receptors, Antigen, T-Cell, alpha-beta; C045084:invariant chain; D015847:Interleukin-4; D007371:Interferon-gamma