脳内Hybrid Resistanceとその抗腫瘍機序に関する実験的検討

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A Moloney virus-induced T cell lymphoma, YAC-1, derived from A/Sn (H-2^a) inbred mouse origin, was tested for hybrid resistance (HyR) after subcutaneous (s.c.) or intracerebral (i.c.) tumor cell inoculation into syngeneic and semi-syngeneic mice. The F1 hybrids (H-2^<a/b>) between A/Sn and C57BL/6 mice more strongly resisted the s.c. inoculation of 10^6 and 5 × 10^5 cells than did syngeneic recipients. In contrast, no HyR to the i.c. inoculation of 10^4 and 10^3 cells was seen in the F1 hybrid mice. Natural killer (NK) cell activity was much higher in F1 hybrids than in syngeneic mice. ^<125>I-iododeoxyuridine-labeled YAC-1 cells were more efficiently eliminated from the highly resistant F1 hybrids than from the parental strain in both 4 and 18 hour in vivo rejection assays via intravenous (i.v.) and s.c. injection, respectively. The remaining radioactivity of the brain, however, did not differ between these mice. Thus, there was a correlation between the in vivo resistance of F1 hybrid mice to challenge s.c. inoculation of parental tumors and their expression of lymphocyte-mediated natural cytotoxicity in vitro against those tumors. T cell depletion by thymectomy followed by irradiation and fetal liver reconstitution did not abrogate the s.c. HyR against YAC-1, whereas NK cell depletion by i.v. administration of anti-asialo-GM1 antibodies resulted in the disappearance of the resistance. Furthermore, genotypic study segregating (A/Sn × C57BL/6) F1 × A/Sn backcross mice indicated that the s.c. HyR might be attributable primarily to heterozygosity within the H-2 complex. Taken together, it was suggested that HyR to an NK cell-sensitive YAC-1 is mediated by an NK cell-dependent cytotoxic effector mechanism with H-2-linked genetic control against s.c. tumor grafts, while such an NK cell-mediated natural resistance does not operate in the brain.
日本脳神経外科学会の論文
1990-11-01

脳内Hybrid Resistanceとその抗腫瘍機序に関する実験的検討

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