title: Association of intermediate T cell receptor cells, mainly their NK1.1(-) subset, with protection from malaria.
abstract: Mice were infected with Plasmodium (P.) yoelii blood-stage parasites. Both the liver and spleen were the sites of inflammation during malarial infection at the beginning of day 7. The major expanding cells were found to be NK1.1(-) intermediate alphabetaTCR (alphabetaTCR(int)) in the liver and spleen, although the population of NK1.1(+) alphabetaTCR(int) cells remained constant or slightly increased. These TCR(int) cells are of extrathymic origin or are generated by an alternative intrathymic pathway and are distinguished from conventional T cells of thymic origin. During malarial infection, the population of conventional T cells did not increase at all. TCR(int) cells purified from the liver of mice which had recovered from P. yoelii infection protected mice from malaria when they were transferred into 6.5-Gy-irradiated mice. Interestingly, the immunity against malaria seemed to disappear as a function of time after recovery, namely, mice which had recovered from malaria 1 year previously again became susceptible to malarial infection. The present results suggest that TCR(int) cells are intimately associated with protection against malarial infection and, therefore, that mice which had recovered from malaria 1 year previously lost such immunity.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Niigata, 951-8510, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Weerasinghe
authors.forename: H
authors.initials: H
authors.lastname: Sekikawa
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Mannoor
authors.forename: S R
authors.initials: SR
authors.lastname: Morshed
authors.forename: R C
authors.initials: RC
authors.lastname: Halder
authors.forename: T
authors.initials: T
authors.lastname: Kawamura
authors.forename: T
authors.initials: T
authors.lastname: Kosaka
authors.forename: C
authors.initials: C
authors.lastname: Miyaji
authors.forename: H
authors.initials: H
authors.lastname: Kawamura
authors.forename: S
authors.initials: S
authors.lastname: Seki
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology*; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex / Q000276:immunology*; D007156:Immunologic Memory / Q000276:immunology; D037181:Lectins, C-Type; D008099:Liver / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008288:Malaria / Q000276:immunology* / Q000517:prevention & control; D051379:Mice; D008810:Mice, Inbred C57BL; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010641:Phenotype; D010967:Plasmodium yoelii / Q000276:immunology*; D011506:Proteins / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D015375:Receptors, Interleukin-2 / Q000276:immunology; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013997:Time Factors
chemical_list: D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D017252:CD3 Complex; 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; D015375:Receptors, Interleukin-2