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A marked increase in natural killer (NK) activity is observed with lymphoid cells prepared from SJL/J mouse spleen and lymph nodes, in which a transplantable reticulum-cell neoplasm (RCN) is growing. The killer cells are non-adherent, non-phagocytic, relatively resistant to X-ray, and scarcely or only partially inactivated by treatment with anti-Thy 1.2 serum and complement. The killer activity is directed against a wide variety of tumor target cells, not requiring homology in histocompatibility, but is selective and not indiscriminate. Kinetics of in vivo development on NK activity, competitive inhibition of in vitro cytotoxicity by target cells and their membrane extracts are described. The NK activity appears to increase in parallel with the infiltration and growth of RCN in these organs. No such augmented NK activity was observed with other types of tumors that grew in these organs of SJL/J mice. (C57BL/6 X SJL/J)F1 mice pretreated with silica to abrogate Hh restriction and subsequently injected with RCN of SJL/J (H-2s) origin supported the growth of transplanted RCN. The high NK activity associated with this RCN was markedly reduced by in vitro treatment with anti-H2b serum plus complement, indicating the host origin of NK cells. However, the close association of RCN growth with elevated NK activity may indicate a special function of RCN in promoting NK activity by an unknown mechanism(s) of cellular interactions.

Abstract. This report describes a trans-species rescue of defective MSV genome with helper leukemia virus derived from cats. This rescue was achieved by in vitro co-cultivation of hamster tumor cells with feline embryo cells in the presence of helper feline leukemia virus (FeLV), or by inoculation of tumor cells into FeLV-infected newborn cats.The rescued focus-forming viruses produced foci in feline embryo cultures but not in cultures of mouse, rat, and hamster species. One isolate was tested and found to induce sarcoma in a kitten. Antigenic and viral interference studies indicated that the focus-forming virus has the viral envelope of FeLV. Virus stocks consisted of a mixture of focus-forming particles and a 1000-fold excess of helper FeLV. Virus assay patterns in feline embryo cultures with or without added helper FeLV indicated that this helper virus is required for the transformation of feline cells.