RELATIVE CONTRIBUTION OF ANTIPROLIFERATIVE AND HOST IMMUNITY-ASSOCIATED ACTIVITY OF MOUSE INTERFERON IN MURINE TUMOR-THERAPY

  • 1 January 1984
    • journal article
    • research article
    • Vol. 44  (12) , 5661-5665
Abstract
Administration of mouse interferon (IFN; 0.5 to 1 .times. 107 reference units/mg protein) inhibited the growth of Meth A and Meth 1 fibrosarcomas, but to a lesser extent, if at all, the growth of Colon 26 adenocarcinoma in BALB/c mice. The in vitro IFN sensitivity of these 3 tumors was not consistent with the in vivo therapeutic response in mice bearing these tumors under the present experimental conditions; Colon 26, the most sensitive of the 3 tumors in the in vitro antiproliferation test, did not respond or responded most poorly to IFN therapy; Meth A and Meth 1 tumors responded similarly well to IFN therapy, although there was about a 100-fold difference in their in vitro IFN sensitivity. These results as well as the kinetic analysis of IFN concentrations of the serum of Meth A- or Colon 26-bearing mice did not indicate that the antiproliferative activity of IFN was solely responsible for its in vivo therapeutic effect. In contrast, abrogation of T-cell immunity by .alpha. mouse thymocyte globulin completely nullified the IFN-dependent therapeutic effect in Meth A-bearing mice. The IFN-dependent therapeutic response in Meth A tumors was much weaker in T-cell-defective BALB/c (nu/nu) mice than that in immunologically competent BALB/c (+/+) mice and was marginal, if present at all, confirming that T-cell immunity was involved in the IFN-dependent therapeutic effect and suggesting that the antiproliferative activity of IFN may only be responsible to a small extent for the therapeutic effect.