DIFFERENTIAL ACTIVATION REQUIREMENTS OF CLONED T CELLS

克隆 T 细胞的差异激活要求

• 批准号: 3137650
• 负责人: Rosemarie H DeKruyff
• 金额: $ 10.17万
• 依托单位: LUCILE SALTER PACKARD CHILDREN'S HOSP
• 依托单位国家: 美国
• 财政年份: 1986
• 资助国家: 美国
• 起止时间: 1986-09-01 至 1989-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3137650
• 关键词: B lymphocyte; T lymphocyte; antibody formation; antigens; cell cell interaction; cell population study; clone cells; density gradient ultracentrifugation; flow cytometry; helper T lymphocyte; histocompatibility antigens; hybridomas; immunochemistry; immunotherapy; interleukin 2; leukocyte activation /transformation; macrophage; macrophage activating factor; radiotracer; suppressor T lymphocyte

The goal is to gain further insight into mechanisms governing T cell activation and its regulation. To this end, a large panel of L3T4+ inducer T cell clones has been generated. These clones display distinct differences in their requirements for activation. For example, some clones respond to antigen presented either by macrophages or B cells, while others respond to antigen presented by macrophages but not by B cells. Some clones respond to determinants present on B cells but not macrophages. Several of the nominal antigen specific T cell clones are also reactive against allogeneic MHC and Mls determinants. Using these clones I propose to: 1) examine T cell clones which fail to proliferate in response to antigen presented by B cells in order to determine a) how their activation requirements differ from those of T cell clones which do respond to antigen presented by B cells and b) how these two types of clones differ in their ability to induce antibody synthesis; 2) examine in detail the activation of T cell clones by Mls determinants and attempt to characterize these determinants; 3) examine mechanisms regulating the activation of NP-specific inducer T cells by analyzing their inhibition by NP-specific suppressor factors derived from NP-specific suppressor T cell hybridomas. This proposal will attempt to increase our understanding of the molecular and cellular interactions governing T cell activation and its suppression. Such an understanding is vital to the favorable manipulation of the immune system in many disease states.

目标是进一步了解T细胞的调控机制， 激活及其调节。 为此，使用了大量L3 T4+诱导剂， 已经产生了T细胞克隆。 这些克隆体表现出明显的 他们对激活的要求不同。 例如，一些克隆 对巨噬细胞或B细胞呈递的抗原有反应，而其他 对巨噬细胞呈递的抗原有反应，但对B细胞无反应。 一些 克隆对存在于B细胞而不是巨噬细胞上的决定簇有反应。 几种标称抗原特异性T细胞克隆也是反应性的 针对同种异体MHC和Mls决定簇。 使用这些克隆，我建议： 1)检查不能响应抗原增殖的T细胞克隆 为了确定a）它们的激活如何 这些要求不同于对抗原应答的T细胞克隆 B）这两种类型的克隆在它们的表达上如何不同， 诱导抗体合成的能力; 2)详细检查Mls决定簇对T细胞克隆的激活 并试图描述这些决定因素; 3)检查调节NP特异性诱导物T的活化的机制 通过分析NP特异性抑制因子对细胞的抑制作用 来源于NP特异性抑制性T细胞杂交瘤。 这项建议将试图增加我们对分子生物学的理解。 以及控制T细胞活化及其抑制的细胞相互作用。 这样的理解是至关重要的有利操纵免疫 在许多疾病中。