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Defects in cell‐mediated immunity during growth of a syngeneic simian virus‐induced tumor
Author(s) -
Howell Stephen B.,
Dean Jack H.,
Law Lloyd W.
Publication year - 1975
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910150118
Subject(s) - immune system , immunity , spleen , virus , neoplasm , biology , antigen , lesion , tumor antigen , cancer research , immunology , effector , virology , pathology , medicine , immunotherapy
Four assays of tumor‐specific cell‐mediated immunity were compared during growth of a syngeneic Simian‐virus‐40‐induced tumor, mKSA. Major differences were found in immunity detected by the tumor neutralization test (the Winn test), direct tumor challenge, the microcytotoxicity assay and the 51 chromium‐release lymphocytotoxicity assay. Progressive growth of the neoplasm followed by loss of immunity (the eclipse phenomenon) was documented with the Winn test. It was established that this eclipse phenomenon represented a lesion in the T‐cell system of tumor‐bearing hosts. This lesion was found to be specific and unrelated to anatomic tumor location. The ability to produce graft‐versus‐host reactions, and the ability to respond to mitogens, were found to be generally intact in tumor‐bearing animals. Cells capable of recognizing mKSA tumor antigens and reconstituting an immune response following surgical removal of tumor or upon transfer to normal mice were found in the spleens of mice bearing advanced tumors. No suppressor cells that might account for the eclipse phenomenon could be demonstrated. Tumor‐bearer serum did not block neutralizing activity of immune spleen cells in the Winn test, and immune cells were capable of neutralizing tumor even in tumor‐bearing hosts. The possibility that the lesion is intrinsic to T‐cell precursors of effector cells is discussed.