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  • Title: The anti-tumor effects of IL-12 involve enhanced IFN-gamma production by anti-tumor T cells, their accumulation to tumor sites and in situ IFN-gamma production.
    Author: Fujiwara H, Hamaoka T.
    Journal: Leukemia; 1997 Apr; 11 Suppl 3():570-1. PubMed ID: 9209457.
    Abstract:
    We investigated cellular and molecular mechanisms underlying the anti-tumor effects of IL-12. Intraperitoneal injections of rIL-12 into later stages of tumor-bearing mice induced not only a striking reversal of suppressed IFN-gamma-production by splenic T cells, but also complete regression of s.c. growing tumors. A massive infiltration of lymphoid cells was found following IL-12 treatment. Whereas fresh spleen cells obtained from IL-12-treated tumor-bearing mice failed to express IFN-gamma mRNA, significant levels of IFN-gamma mRNA were detected in the tumor mass of the same mice. The systemic administration of anti-IFN-gamma antibody (Ab) prior to IL-12 injection abrogated the anti-tumor effect of IL-12 although this Ab did neither inhibit accumulation of lymphoid cells to tumor sites nor in situ IFN-gamma expression. Importantly, while high levels of inducible nitric oxide synthase (iNOS) mRNA expression was induced in tumor masses after IL-12 treatment, its expression was completely inhibited by pretreatment with anti-IFN-gamma Ab. Thus, induction of tumor regression by IL-12 is ascribed to a series of events: a striking reversal of suppressed IFN-gamma production by anti-tumor T cells, their accumulation and IFN-gamma production at tumor sites, and manifestation of IFN-gamma activity as exemplified by iNOS expression.
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