MECHANISM OF THE H-2 EFFECT ON VIRAL LEUKEMOGENESIS

H-2型小鼠已在几种不同的病毒中得到证实。 系统在确定易感性或 对MuLV相关白血病的抗性，很明显， 小鼠的免疫系统是这种H-2效应的主要介质， 它对病毒免疫反应的影响 和/或肿瘤抗原。 根据病毒/宿主组合的不同， 各种研究表明，H-2效应在不同的次区域都有分布， 的H-2复合物，这表明，有缺陷的反应的一部分， 免疫系统的不同成分可能是 敏感性（即，在不同的情况下，有缺陷的电阻。 具有 广泛研究了细胞毒性T淋巴细胞（CTL）反应， H-2-同源BALB/c小鼠品系与同源Friend和Gross 病毒诱导的肿瘤，我们现在建议扩大我们的方法，包括 辅助性T淋巴细胞和抑制性T淋巴细胞参与免疫调节的研究 H-2相关白血病耐药现象。 有待探讨的方法 包括：通过淋巴细胞亚群转移肿瘤抗性， 辅助性T淋巴细胞反应及其参与免疫调节的研究 CTL的产生和抗体产生、增殖实验 用同源肿瘤细胞作为刺激物， 探讨T细胞抑制可能参与 H-2b/H-2d杂合子无反应性（与H-2b相比 纯合子）与H-2b-纯合子FV肿瘤细胞。

The H-2 type of mice has been demonstrated in several different viral systems to play an important role in determining the susceptibility or resistance to MuLV-associated leukemogenesis, and it is clear that the immunologic system of the mouse is the major mediator of this H-2 effect by its influence on the occurrence of an effective immune response to viral and/or tumor antigens. Depending on the virus/host combinations used in various studies, the H-2 effect has proved to map in different subregions of the H-2 complex, suggesting that defective responses on the part of different components of the immune system may be the basis for susceptibility (i.e., defective resistance) in different cases. Having extensively studied the cytotoxic T lymphocyte (CTL) response in H-2-congenic BALB/c mouse strains to syngeneic Friend and Gross virus-induced tumors, we now propose to expand our approach to include the study of helper T lymphocyte and suppressor cell participation in the H-2-associated leukemia resistance phenomenon. Methods to be explored include: transfer of tumor resistance by lymphocyte subsets, generation of helper T lymphocyte responses and study of their participation in the generation of CTL and in antibody production, proliferation experiments with syngeneic tumor cells as stimulators, and diverse experiments designed to explore the possible involvement of T cell suppression in the nonresponsiveness of H-2b/H-2d heterozygotes (by comparison with H-2b homozygotes) to H-2b-homozygous FV tumor cells.