HOST REGULATION OF IGE SYNTHESIS IN MURINE HYBRIDOMAS

本申请中提出的研究将调查通过哪些机制 宿主对分泌IgE杂交瘤细胞的免疫应答 在特异性调节IgE的表达上。我早期的研究表明 证明在BALB/c小鼠体内传代过程中，IgE-- 小鼠杂交瘤B53的产生诱导效应细胞的发育 在宿主中，这似乎反过来似乎调节B53中IgE的合成 通过一种依赖于宿主T的存在的机制 淋巴细胞。进一步证实了对IgE合成的抑制 这是由于抑制了B53中的epsilon-Heavy链转录 细胞。本研究的目的是调查：1)寄主 参与免疫球蛋白E调节的效应细胞 在产生IgE的杂交瘤细胞中合成；2)精确的 在目标杂交瘤细胞中发生的生化和分子事件 导致免疫球蛋白E合成的调节。这些研究具有 有可能确定宿主的确切角色和基本机制 细胞在调节IgE免疫反应中的作用这样的信息将是 与研究免疫反应高度相关，在免疫反应中产生IgE 导致病理后果，如过敏反应和特应性 精神错乱。

Studies proposed in this application will investigate mechanisms by which the immune response of the host to IgE-secreting hybridoma cells results in specific regulation of IgE expression. My earlier studies have demonstrated that during in vivo passage in BALB/c mice, the IgE-- producing murine hybridoma B53 induces the development of effector cells in the host which in turn appear to regulate synthesis of IgE in the B53 cells by a mechanism that is dependent on the presence of host T lymphocytes. Suppression of IgE synthesis has been further demonstrated to be due to inhibition of epsilon-heavy chain transcription in the B53 cells. The aims of the present study are to investigate: 1) the host effector cells participating in and responsible for regulation of IgE synthesis in the IgE-producing hybridoma cells; and 2) the precise biochemical and molecular events that occur in the target hybridoma cells which result in regulation of IgE synthesis. These studies have the potential to identify the precise roles and basic mechanisms of host cells in regulating IgE immune responses. Such information would be highly relevant to studying immune responses in which IgE production leads to pathological consequences, such as anaphylaxis and atopic disorders.