HOST REGULATION OF IGE SYNTHESIS IN MURINE HYBRIDOMAS

本申请中提出的研究将调查 宿主对分泌IgE的杂交瘤细胞的免疫应答导致 特异性调节IgE表达。 我早期的研究 证明了在BALB/c小鼠体内传代过程中，IgE- 产生小鼠杂交瘤B53诱导效应细胞的发育 在宿主中，这反过来似乎调节B53中IgE的合成， 通过依赖于宿主T细胞存在的机制， 淋巴细胞 IgE合成的抑制已被进一步证实 可能是由于B53细胞中ε-重链转录的抑制， 细胞 本研究的目的是探讨：1）宿主 参与并负责调节IgE的效应细胞 在产生IgE的杂交瘤细胞中的精确合成;和 在靶杂交瘤细胞中发生的生物化学和分子事件 其导致IgE合成的调节。 这些研究有 确定宿主的确切作用和基本机制的潜力 细胞调节IgE免疫反应。 这些信息将是 与研究免疫反应高度相关， 导致病理后果，如过敏性反应和特应性 紊乱

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.