Correlation Between Tumor-Specific Systemic and In Situ Immunity as Manifested by the Delayed Hypersensitivity Response23

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Abstract
The delayed hypersensitivity response (DHR) to the transplanted murine mammary adenocarcinoma (T1699) was studied by means of both direct challenge of tumor-bearing DBA female mice and adoptive transfer of DHR to normal DBA/2 female mice with the use of immunocompetent cells. Specific effector cells for DHR were demonstrable in both the host inflammatory cell fraction of the solid tumor and in the peripheral lymph nodes. A significant proportion, but not all of these in situ effector cells, appeared to be derived from thymus cells. The kinetics and specificity of the DHR were studied with both intact tumor cells and a soluble antigen preparation. The DHR’s seen appeared to be tumor-specific. A similar approach was used to investigate the DHR in a series of early passages of spontaneous C3H mammary tumors. As in the T1699 model, DHR effector cells isolated from the host inflammatory cell fraction of the tumor masses and the draining lymph nodes were capable of transferring DHR. There was considerable variation, however, among the different C3H tumors in the relationship between in situ DHR and DHR in the regional lymph nodes. The activity of the in situ effector cells was equivalent to that of the cells from the lymph nodes in 5 of the 12 tumor groups studied. The remaining 7 groups demonstrated a lack of correlation; depending on the tumor line tested, the activity of cells from one site was significantly different from the activity of cells from another site. The pattern of reactivity for a given tumor was consistent following in vivo passage.