THE IMMUNOLOGY OF INCREASED AGGRESSIVENESS OF SJL TUMORS

SJL品系小鼠在移植后自发发展为淋巴瘤 在同基因小鼠中，可以作为惰性肿瘤或侵袭性肿瘤生长。 而惰性肿瘤不断地有转化为 侵袭型、侵袭性肿瘤保持侵袭性。这个 SJL淋巴瘤侵袭性增加与缺乏 H-2DS，I类主要组织相容性复合体(MHC)抗原 肿瘤细胞表面。在此，建议检验以下假设： H-2DS阴性(D-)SJL淋巴瘤侵袭性增加可能在 部分，归因于：1)细胞毒对D-肿瘤细胞的杀伤作用不足 T淋巴细胞(CTL)作为肿瘤优先识别的结果 与H-2DS相关的CTL抗原；2)识别和/或缺陷 自然杀伤细胞对D-肿瘤细胞的杀伤作用，或3)更大 D-肿瘤细胞对淋巴因子刺激的敏感性 合成的是伴随着T细胞增殖的结果 大多数SJL淋巴瘤的生长或D淋巴瘤更倾向于 诱导这种淋巴因子的合成。由于类似的增长， 在一些人类淋巴瘤的发展过程中可以看到侵袭性，它 希望这项研究的结果将促进对损失的调查 I类MHC抗原作为人类潜在的预后指标。(MI)

SJL strain mice spontaneously develop lymphomas which, upon transplantation in syngeneic mice, can grow either as indolent or aggressive tumors. Whereas indolent tumors are at constant risk of conversion to the aggressive type, aggressive tumors maintain their aggressiveness. The increase in aggressiveness of SJL lymphomas correlates with absence of H-2Ds, class I major histocompatibility complex (MHC) antigen from the tumor cell surface. It is, herein, proposed to test the hypothesis that the increased aggressiveness of H-2Ds negative (D-) SJL lymphomas may, in part, be attributed to: 1) deficient killing of D-tumor cells by cytotoxic T lymphocytes (CTL) as a consequence of preferential recognition of tumor antigen by CTL in association with H-2Ds; 2) deficient recognition and/or killing of D-tumor cells by natural killer cells, or; 3) a greater sensitivity of D-tumor cells to the stimulatory influence of lymphokines synthesized as a consequence of the T cell proliferation which accompanies the growth of most SJL lymphomas or a greater propensity of D-lymphomas to induce synthesis of such lymphokines. Since a similar increase in aggressiveness is seen during the progression of some human lymphomas, it is hoped that the results of this study will spur investigation of loss of class I MHC antigen as a potential prognostic indicator in humans. (MI)