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Department of Immunology Research, Roswell Park Memorial Institute,3 Buffalo, New York 14263
We report that the injection of goat anti-Th-B antibody reagent (antiserum raised against BALB/c myeloma MOPC 104E cells and purified) into AKR mice results in significant enhanced growth of the allogeneic Sarcoma 180. This effect on tumor growth is transferred by the injection of spleen or thymus cells derived from tumor-bearing animals treated with anti-Th-B into tumor recipients. Cells transferred from the thymus are more effective than are cells transferred from the spleen.
The tumor-enhancing effect of administration of the anti-Th-B reagent does not appear to be due to an effect on cytotoxic effector cells or their precursors since in vitro experiments showed that such effector cells against EL-4 cells are not affected by the anti-Th-B reagent. Absorption of minute amounts of anti-Th-B antibody by tumor cells may contribute somewhat to the growth enhancement, although Sarcoma 180 cells do not bind significant amounts of anti-Th-B antibodies, as shown by their inability to remove anti-Th-B antibodies cytotoxic for MOPC 104E cells.
The tumor-enhancing effect of administration of the anti-Th-B antibodies appears to be due to the stimulation of particular T-cells, i.e., suppressor T-cells, since we show that the transfer of thymus cells from the anti-Th-B-treated mice is more effective than the transfer of spleen cells. Moreover, it is unlikely that transfer of effector T-cells in any amount could affect the tumor growth in the host except to cause decreased growth, since the host already has its own effective complement of effector cells before any transfer of cells from the anti-Th-B-treated animal.
It appears therefore that suppressor T-cells may well be an important factor in the tumor enhancement caused by administration of anti-Th-B antibodies although other mechanisms, humoral or cellular, may also be effective. We suggest that a precursor of suppressor cells carries the Th-B determinant and that anti-Th-B antibodies stimulate these precursor cells into mature active suppressor cells that depress the cellular immune mechanism involved in the rejection of Sarcoma 180 in AKR mice.
1 Supported by Grants CA-14562 and CA-17609, awarded by the National Cancer Institute, Department of Health, Education and Welfare.
2 On leave of absence from the Department of Biochemistry, Kyushu University School of Dentistry, Katakasu Fukuoka, Japan.
3 A unit of the New York State Department of Health.
Received 1/26/77. Accepted 5/26/77.
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