Various numbers of spleen cells from specifically immunized mice were mixed with constant numbers of target tumor cells, and were inoculated subcutaneously into thymectomized, x-irradiated recipients. Small numbers of admixed immune spleen cells produced a statistically significant, and reproducible, acceleration of tumor growth in the inoculum as compared with controls of either nonimmune spleen cells or spleen cells from animals immune to a different, non-cross-reacting, tumor. Larger. numbers of specifically immune spleen cells, however, produced inhibition of tumor growth. These data imply that the normal immune reaction may have a dual function in relation to neoplasia: (i) stimulation of tumor growth, early in the course of the disease, or whenever the immune reaction is minimal; (ii) inhibition of tumor growth at other times.

The strain distribution pattern of five different post-thymectomy autoimmune diseases was determined in 21 inbred and two congenic, resistant strains of mice. The results indicated that susceptibility genes outside the H-2 complex may be involved in the development of localized autoimmune diseases in neonatally thymectomized mice. Studies of recombinant inbred strains also showed that susceptibility to gastritis was not associated with the H-2 haplotype but appeared to be influenced by a minor histocompatibility locus. Possible linkage to the H-2 complex was suggested only in the development of coagulating gland adenitis. Although one experiment showed that susceptibility to orchitis and coagulating gland adenitis was inherited as a recessive trait, further studies are required to determine the exact mode of inheritance in each disease system.

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