title: Spleen cell transfer induces T cell-dependent granulomas in tuberculous nude mice.
abstract: After IV infection with an attenuated strain of Mycobacterium bovis BCG, athymic nude mice produced a few hepatic granulomas; most of the other foci of bacterial parasitization lacked obvious cellular reactions. Nude mice BCG-infected four weeks earlier received spleen cells from normal euthymic littermates. After transient splenomegaly which peaked at about two weeks, numerous hepatic granulomas appeared by four weeks and the number of viable BCG decreased. The development of hepatic granulomas required viable spleen cells and depended on the spleen cell dose and corresponded with positive footpad reactions. The effective population seemed to be T cells, since they were sensitive to treatment with anti-brain associated theta antigen serum (antiBAT) plus complement, and were found in nylon-wool passed fractions. After transfer with sensitized spleen cells, adoptive immunity was observed, provided that the recipient BCG-infected nude mice had been splenectomized before transfer. AntiBAT plus complement treatment of the sensitized spleen cells decreased the granuloma-producing as well as antimycobacterial capacity. When BCG-infected nude mice were irradiated with 500 r of gamma ray, granuloma production was decreased after immune spleen cell transfer. Co-transfer of immune spleen cells with normal nude mouse bone marrow cells to BCG-infected irradiated nude recipients restored the granuloma-forming ability.
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells; D005260:Female; D006099:Granuloma / Q000209:etiology*; D007111:Immunity, Cellular; D007116:Immunization, Passive; D008107:Liver Diseases / Q000209:etiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C / Q000276:immunology; D008819:Mice, Nude / Q000276:immunology*; D009163:Mycobacterium bovis / Q000472:pathogenicity; D013154:Spleen / Q000637:transplantation*; D013601:T-Lymphocytes / Q000276:immunology* / Q000637:transplantation; D014376:Tuberculosis / Q000209:etiology*