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Cell-mediated responses in dogs with spontaneous neoplasms. I. Detection of cell-mediated cytotoxicity by the chromium-51 release assay.

A series of 43 dogs with spontaneous melanomas, sarcomas, or mammary carcinomas were tested for peripheral blood lymphocytotoxicity against a range of allogeneic tumor cells in vitro on one or more occasions during therapy. All tumor-bearer groups contained a proportion of dogs showing a significant 51Cr release with increasing effector-to-target cell ratios. However, cytotoxicity was not restricted for target cells of the same histologic type as that of the effector cell donor. Some unrelated target cells more sensitive to nonspecific effects showed a greater cytotoxicity in some instances. Control effector cells from healthy dogs were nonspecifically cytotoxic for a range of tumor target cells in a similar proportion of instances. Short-term cultures of autochthonous tumor target cells were resistant to lysis in the 51Cr release assay. The findings did not provide evidence for the existence of specific tumor antigens operative to allogeneic 51Cr release cytotoxicity assays.

Animals↗

Cell-mediated T lymphocyte responses against syngeneic cells modified with amino-reactive hapten (AED-NH2): H-2Dk serves as an element for cell-mediated lympholysis to amino-reactive hapten (AED-NH2)-modified self.

Spleen cells from C3H/He mice immunized to the newly synthesized amino-reactive hapten, 5-sulfo-1-naphthoxy acetic acid N-hydroxysuccinimide (AED-NH2), were stimulated in vitro with AED-NH2 modified syngeneic cells. After 5 days of culture, effector cells were assayed for their cytotoxic activity against AED-NH2-modified target blast cells. In contrast to other amino-reactive haptens reported so far, a strong cytotoxic activity against AED-NH2-modified syngeneic cells was found in H-2b mice as well as in H-2k mice. Furthermore, Dk-restricted anti-AED-NH2 CTL recognition was observed in H-2k mice as shown by cold target inhibition. Previous studies have demonstrated the predominant influence of K over D region self determinants, and of the chemical reactivity of the haptenic reagent in Ir gene control of CTL response to hapten-self. The present report illustrates the importance of the hapten itself in genetic regulation of these CTL responses.

Animals↗