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Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 200142
Host immunity to a growing antigenic solid tumor was studied with a transplanted methylcholanthrene-induced sarcoma (MCA-25) in inbred female strain 2 guinea pigs. Tumor-specific cellular immunity was evaluated in vivo by delayed cutaneous hypersensitivity reactions to a transplantation antigen extract of the tumor and in vitro by splenic lymphocyte-mediated cytoxicity.
Animals receiving 100,000 MCA-25 cells i.m. demonstrated tumor-specific cellular cytotoxicity from 7 days to the conclusion of the study 28 days after tumor transplant. Tumors were 10% body weight at this time. MCA-25-bearing animals had a degree of tumor-specific cellular cytotoxicity similar to those of guinea pigs "hyperimmunized" to the MCA-25 antigen.
Guinea pigs presensitized to dinitrochlorobenzene developed a delayed cutaneous hypersensitivity reaction to a dinitrochlorobenzene challenge in the presence of a growing MCA-25 tumor. Animals 7 and 14 days after tumor transplant developed a delayed cutaneous hypersensitivity reaction to MCA-25 antigen extract. Animals with tumors larger than 1 cm reacted to dinitrochlorobenzene but minimally to the tumor antigen. To explain the discrepancy between in vitro and in vivo detectable tumor-specific cellular immunity in animals with tumors larger than 1 cm, we evaluated the effects of serum from these animals on cellular cytotoxicity. Serum from animals with palpable MCA-25 tumors completely inhibited MCA-25-specific cellular cytotoxicity but not cellular cytotoxicity directed against another methylcholanthrene-induced tumor. Studies with serum from animals bearing 1- to 1.5-cm tumors suggested that this inhibition was mediated, at least in part, by antibody directed against the MCA-25 tumor-specific antigen.
1 Present address: Department of Surgery, Massachusetts General Hospital, Boston, Mass. 02114.
2 Requests for reprints to this address.
Received 1/27/72. Accepted 8/ 1/72.
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