The role of cellular and humoral immunity in the localization of blood-borne, bone marrow-derived ADCC effector cells into the T1699 mammary adenocarcinoma was investigated. Administration of ALG before tumor inoculation caused total immunosuppression and resulted in minimal in situ inflammation. ALG treatment started at the time of tumor inoculation suppressed the delayed hypersensitivity response below a detectable level but permitted a significant antibody response. Under these circumstances, the localization of ADCC effector cells into the tumors appeared normal. Similarly, administration of ALG at later stages of tumor growth, where ALG acts as an anti-inflammatory agent, did not interfere with the normal infiltration of ADCC effector cells in situ, although the delayed hypersensitivity response was totally suppressed. When melphalan treatment was used to produce tumor-bearing mice with an intact delayed hypersensitivity response but devoid of a significant antibody response, the drug-treated animals were found to have high levels of ADCC effector cells in situ. These results demonstrate that although the in situ inflammatory reaction appears to be immunologically dependent, neither the delayed hypersensitivity nor the antibody response is solely responsible for the localization of ADCC effector cells in the T1699 mammary tumor.


This work was supported by Public Health Service Grant CA-17694 and ACS Grant IM-84.

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