Summary.-The lability of cell surface histocompatibility antigens of 2 murine lymphomata was examined. These 2 tumours differ greatly in their capacity to metastasize in syngeneic hosts. Cells of the metastatic lymphoma released histocompatibility antigens in vivo and in vitro at a greater rate than cells of the nonmetastasizing lymphoma. Antigen/antibody complexes formed by the addition of allo-antiserum to intact cells disappeared more rapidly from the surface of cells of the metastatic line. We propose that the instability of surface antigens may be an integral feature of malignant cells and that there may be a quantitative relationship between the lability of membrane components and the capacity of the tumour to metastasize.

Summary.-The metastatic behaviour of the L5178E (non-M) lymphoma and a highly metastatic subline L51787ES (M) were studied in syngeneic DBA2 mice. The non-M tumour rarely metastasizes in intact syngeneic mice, but produces extensive and rapidly lethal metastases when implanted into irradiated recipients. The metastatic behaviour of the M subline is unaffected by irradiation of the host. By conventional transplantation criteria, the non-M tumour is more immunogenic than the M subline. Both tumours, however, produce similar responses in a lymphnode weightgain assay. Host-cell infiltration of the tumours growing s.c. is much greater in the non-M than the M, the infiltrating cells being Fc-receptor-positive and maturing into macrophages after 2 days in vitro.Although spontaneous in vitro motility of the M cells is much greater than that of the non-M, the metastatic behaviour of the tumours is clearly determined by host immunological responses.

No abstract

DC often require stimulation from CD4+ T cells to propagate CD8+ T cell responses, but precisely how T cell help optimizes the priming capacity of DC and why this appears to differ between varying types of CD8+ T cell immunity remains unclear. We show that CD8+ T cell priming upon HSV-1 skin infection depended on DC receiving stimulation from both IFN-α/β and CD4+ T cells to provide IL-15. This was not an additive effect, but resulted from CD4+ T cells amplifying DC production of IL-15 in response to IFN-α/β. We also observed that increased innate stimulation reversed the helper-dependence of CD8+ T cell priming and that the innate stimulus, rather than the CD4+ T cells themselves, determined how ‘help’ was integrated into the priming response by DC. These findings identify T cell help as a flexible means to amplify varying suboptimal innate signals in DC.