CONTROLS OF PROLIFERATION SPECIFIC FOR LEUKEMIAS

本项目是对小鼠的自然和诱导抗性的研究。 血液性肿瘤的增殖。调查的重点是 免疫生物学与效应系统的异质性；关于调节 机制，以及反应的遗传控制，目标决定因素， 以及效应细胞和调节细胞群体的分化。这个 造血组织相容性(HH)和/或主要 正常人组织相容性复合体(H-2)基因产物的表达 造血干细胞和白血病-淋巴瘤细胞是 自淋巴细胞识别这些结构以来的投射 系统导致体内靶细胞的抑制和/或排斥(即， 杂交种和同种异体抗药性)和体外细胞毒性(即， 原代F1抗亲本细胞介导的淋巴溶解)。重点将是 不仅放置在HH/H-2控制的结构上，也放置在其他细胞上 作为小鼠对自体免疫反应的靶标的结构 或者是同基因肿瘤。这种“自身反应”是由效应器调节的。 属于自然杀伤(NK)和细胞毒性T淋巴细胞(CTL) 上课。辐照F1杂交瘤对亲本淋巴瘤移植物的抗性 小鼠涉及不明的效应器机制，部分是NK样(效应器 不需要被诱导，并且相对抵抗辐射，不依赖胸腺， 受干扰素调节)，但识别特定的HH/H-2基因产物和 在18至96小时内造成移植物排斥反应。人血清白蛋白的体外激活 F1抗亲本CTL涉及不同的机制，因为应答细胞 必须受到刺激，而且对辐射敏感，对胸腺也有依赖。 F1抗亲本CTL识别基因的产物 在某些单倍型和菌株中无法与HH基因区分，但 根据重组分析可以与其他基因区分开来。(磅)

This project is a study of natural and induced resistance of mice to the proliferation of hemopoietic tumors. The investigations are focused on the immunobiology and heterogeneity of effector systems; on regulatory mechanisms, and on genetic controls of responsiveness, target determinants, and differentiation of effector and regulatory cell populations. The identity of hemopoietic-histocompatibility (Hh) and/or major histocompatibility complex (H-2) gene products expressed on normal hemopoietic stem cells and leukemia-lymphoma cells is central to the project since recognition of these structures by cells of the lymphoid system leads to inhibition and/or rejection of target cells in vivo (i.e., hybrid and allogeneic resistance) and to cytotoxicity in vitro (i.e., primary F1 antiparent cell-mediated lympholysis). Emphasis will be placed not only on Hh/H-2-controlled structures but also on other cellular structures that serve as targets for mouse reactivities against autologous or syngeneic tumors. Such "autoreactivities" are mediated by effectors belonging to the natural killer (NK) and cytotoxic T lymphocyte (CTL) classes. Resistance to parental lymphoma grafts by irradiated F1 hybrid mice involves unidentified effector mechanisms, in part NK-like (effectors need not be induced and are relatively radioresistant, thymus independent, modulated by interferon), yet recognizing specific Hh/H-2 gene products and causing graft rejection within 18 to 96 hrs. The in vitro activation of F1 antiparent CTL involves different mechanisms, since responder cells must be stimulated and are radiosensitive as well as thymus dependent. F1 antiparent CTL recognize the products of genes that are indistinguishable from Hh genes in certain haplotypes and strains but are distinguishable in others according to recombinant analysis. (LB)