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The Immune Recognition of Ta3 Tumors, Its Facilitation by Endotoxin, and Abrogation by Abcites Fluid¹

From the Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania

Abstract

The escape of TA3-Ha cell line from immune recognition and rejection is not due to complete loss of major histocompatibility antigens, since hyperimmunization with this cell line rendered mice highly resistant against the specific TA3-St line, and vice versa. Sensitization of TA3-Ha-tolerant mice with incompatible skin graft from strain A mice rendered them refractory to TA3-Ha inocula. Accordingly, both the TA3-St and TA3-Ha lines share major histocompatibility antigens. Spleen cells from immunized animals as well as from animals bearing the tumor adoptively transferred tumor resistance into normal mice. This shows that in the non-pretreated, tumor-bearing animal, the escape mechanism can operate in spite of an existing immunogenic stimulus. If this immune stimulus is further incremented by previous injection of 1 µg bacterial endotoxin, the host is sufficiently assisted to defeat a lethal dose of tumor inoculum. The results reported here also indicate that the escape may be aided by ascites fluid. It has been found that components of ascites fluid from C57BL/10Sn or ICR mice carrying TA3-Ha tumor could increase the take of TA3-Ha tumor in normal mice of the same strain.

Footnotes

¹ This study was supported by a grant from the New York Cancer Research Institute, Inc., 1225 Park Avenue, New York, N. Y. and by an institutional grant from the American Cancer Society.