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中文摘要
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本提案的目的是详细了解 由此T细胞帮助B细胞对抗原作出反应。 我们 特别感兴趣的两个过程发生;第一, 启动B细胞应答的事件,其次, 淋巴因子B细胞刺激因子-1(BSF 1)的B细胞。 虽然淋巴因子本身可以驱动B细胞对 B细胞对许多抗原的某些抗原反应,特别是 那些出生在蛋白质上的,需要载体特异性T细胞的存在, 细胞以及淋巴因子。 这些T细胞似乎参与了 主要是在B细胞应答开始时。 它们可以 通过分泌一些迄今未发现的淋巴因子或通过 它们自身的膜蛋白与T细胞上的配体直接接触, 或B细胞和/或分离的膜蛋白,我们计划 研究这些可能性中哪一个是正确的。 膜 待研究的组分将包括T细胞受体,L3 T4, LFA-1和II类分子。 例如,我们将隔离 来自特定辅助性T细胞杂交瘤的受体,并通过 这些受体是否结合抗原, MHC。 这些受体将用于脂质体或之后 转移到另一个T细胞杂交瘤中以检测抗原特异性 辅助活动 BSF 1对B细胞具有多种作用。 它诱导Ia合成 在静息细胞中,并刺激亚最大限度地增殖 活化的B细胞。 我们计划在B上分离BSF 1的受体 细胞,并详细研究这种淋巴因子的诱导作用 没有休眠细胞
英文摘要
The aims of this proposal are to understand in detail the means whereby T cells help B cells respond to antigen. We are particularly interested in two processes which occur; first, the events which initiate B cell response and secondly, the effects on B cells of the lymphokine B cell stimulating factor-1 (BSF1). Although lymphokines alone can drive the responses of B cells to some antigens responses of B cells to many antigens, particularly those born on proteins, require the presence of carrier-specific T cells as well as lymphokines. These T cells appear to be involved chiefly at the beginning of the B cell response. they may be acting by secreting some hitherto undiscovered lymphokine or by direct contact of their own membrane proteins with ligands on T or B cells and/or isolated membrane proteins, we plan to investigate which of these possibilities is correct. Membrane components to be studied will include the T cell receptor, L3T4, LFA-1 and Class II molecules. For example, we will isolate receptors from a particular helper T cell hybridoma and test by various strategies whether these receptors bind antigen plus MHC. These receptors will be used in liposomes or after transfer to another T cell hybridoma to test for antigen-specific helper activity. BSF1 has a number of effects on B cells. It induces Ia synthesis in resting cells, and stimulates proliferation of sub-maximally activated B cells. We plan to isolate the receptor for BSF1 on B cells, and study in detail the inductive effects of this lymphokine no resting cells.
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Project 3: Epitope Selection in Type 1 Diabetes
Molecular Mechanisms of MHCII Recognition by CD8 T Cells in HIV Non-Progressor Patients
  • 批准号:
    9241343
  • 项目类别:
  • 资助金额:
    $27.74万
  • 财政年份:
    2016
  • 负责人:
    JOHN W KAPPLER
  • 依托单位:
Molecular Mechanisms of MHCII Recognition by CD8 T Cells in HIV Non-Progressor Patients
  • 批准号:
    9141956
  • 项目类别:
  • 资助金额:
    $15.85万
  • 财政年份:
    2016
  • 负责人:
    JOHN W KAPPLER
  • 依托单位:
BASIC IMMUNE MECHANISMS & IMMUNOLOGY DISEASE
  • 批准号:
    3530602
  • 项目类别:
  • 资助金额:
    $5.92万
  • 财政年份:
    1988
  • 负责人:
    JOHN W KAPPLER
  • 依托单位:
海外基金