Activation of “eclipsed” lymphoid cells from advanced tumor-bearing mice through adoptive transfer to sublethally irradiated syngeneic hosts
- 15 October 1975
- journal article
- research article
- Published by Wiley in International Journal of Cancer
- Vol. 16 (4) , 629-638
- https://doi.org/10.1002/ijc.2910160413
Abstract
Immunologically inactive or “eclipsed” lymphoid cells from advanced tumor-bearing mice were investigated following their adoptive transfer to irradiated syngeneic hosts. Experiments were performed with two syngeneic tumor-host systems: the T5-BALB/c tumor line chronically infected with a low-leukemogenic Rauscher virus variant and the TM1-C3H tumor line developed from a spontaneous C3H/He mouse mammary tumor. In confirmation of our previous data, peritoneal cells (PC) from advanced tumor-bearing mice (EPC) appeared to have lost any capacity to inhibit specifically the growth of corresponding tumor target cells in in vitro colony inhibition (CI) tests, whereas PC from immunized mice (IPC) were perfectly active. When these EPC were adoptively transferred by intraperitoneal inoculation into sublethally irradiated (450R) syngeneic mice in association with respective tumor extracts (TE), the PC from such recipient mice, taken 5 to 13 days later, were nearly as active in in vitro CI tests as were PC from parallel IPC-recipient mice. For this recovery of specific immunological activity following the adoptive transfer of EPC the adjunction of the TE and irradiation of the recipient animals seem important and may be necessary. On the other hand, no specific immunological activity was seen in PC from irradiated mice to which PC from normal mice had been transferred with TE. In addition to the in vitro results, an effect of adoptive transfer of EPC (retardation of tumor growth) was also observed in vivo. It is concluded that the “eclipsed” immunologically inactive state of the EPC in mice bearing advanced tumor is not irreversible and that activation of these cells can occur in vivo under certain conditions helped by the presence of tumor-specific antigenic stimulus.Keywords
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