title: Differences in the phenotypes of cells mediating anti-tumour immunity at various stages of tumour progression in mice.
abstract: In Winn assays, T cells from donors immunized by tumour excision, or from mice with small tumours, mediate rejection of the metastasizing murine fibrosarcoma MC-2. As the mean size of primary tumours in spleen donors increases, the strength of anti-tumour activity declines, until it is frequently undetectable in spleen cells from mice with very large tumour burdens. Loss of splenic anti-tumour activity is coincident with the appearance of cells capable of suppressing an otherwise protective anti-tumour response in Winn assays. This paper defines the phenotypes of T cells mediating immunity against MC-2. Eleven or more days after tumour inoculation the proportions of tumour-bearer splenic leucocytes expressing Ly 1.2 (CD5), Ly 2.2 (CD8a) or L3T4 (CD4) surface antigens were significantly less than similar preparations from normal animals. Depletion of Ly 1.2+ or L3T4+ cells from spleen cells of donors with small tumours, or from donors immunized by tumour excision, diminished protection in the Winn assay. Depletion of Ly 2.2+ cells from these donors had no effect on immunity. In contrast, spleen cells taken from donors with large tumors lost all anti-tumour activity if pretreated with any one of anti-Ly 1.2 or anti-Ly 2.2 or anti-L3T4 antibodies in the presence of complement. These results suggest that cells bearing the Ly 2.2 marker may be important to weak immunity remaining in the spleens of mice with large tumours, but are not critical to strong immunity generated early in tumour growth, nor to that following tumour excision. That is, in addition to an Ly 1.2+, Ly 2.2-, L3T4+ spleen cell subset also seen early in the growth of the MC-2 tumour, a cell population which expresses the Ly 2.2 marker and which is important to anti-tumour immunity emerges late in tumour growth.
authors.affiliation: Department of Clinical Microbiology, School of Medicine, Flinders University of South Australia, Bedford Park.
authors.forename: L A
authors.initials: LA
authors.lastname: Dent
authors.forename: L K
authors.initials: LK
authors.lastname: Spencer
authors.forename: S
authors.initials: S
authors.lastname: Attridge
authors.forename: J J
authors.initials: JJ
authors.lastname: Finlay-Jones
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis / Q000276:immunology; D000950:Antigens, Ly / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology; D005260:Female; D005354:Fibrosarcoma / Q000276:immunology* / Q000473:pathology; D005434:Flow Cytometry; D007109:Immunity; D051379:Mice; D008815:Mice, Inbred Strains; D009367:Neoplasm Staging; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000276:immunology / Q000473:pathology; D010641:Phenotype; D013154:Spleen / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology*; D014916:Whole-Body Irradiation
chemical_list: D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D000950:Antigens, Ly; D003165:Complement System Proteins