REGULATORY MECHANISMS IN THE IMMUNE SYSTEM
REGULATORY MECHANISMS IN THE IMMUNE SYSTEM
批准号:
3480904
负责人:
JOHN W KAPPLER
金额:
$12.21万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1979
资助国家:
美国
项目状态:
已结题
起止时间:
1979-12-01 至 1996-11-30
关键词:
B lymphocyte T cell receptor T lymphocyte affinity chromatography antigens antireceptor antibody autoradiography biological signal transduction cell cell interaction cellular immunity concanavalin A flow cytometry gel electrophoresis genetically modified animals helper T lymphocyte high performance liquid chromatography hybridomas immunoglobulin M immunoregulation interferons interleukin 1 interleukin 2 laboratory mouse laboratory rat leukocyte activation /transformation leukocyte adhesion molecules liposomes lymphokines major histocompatibility complex membrane activity membrane proteins monoclonal antibody neoplastic cell culture for noncancer research tissue /cell culture
中文摘要
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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