KILLER CELL SURFACE ANTIGENS--BIOCHEMISTRY AND FUNCTION
杀伤细胞表面抗原——生物化学和功能
基本信息
- 批准号:3174706
- 负责人:
- 金额:$ 16.28万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1987
- 资助国家:美国
- 起止时间:1987-08-01 至 1991-09-30
- 项目状态:已结题
- 来源:
- 关键词:T lymphocyte antiidiotype antibody cytolysis flow cytometry human subject interleukin 2 laboratory mouse laboratory rabbit leukocyte activation /transformation leukocyte adhesion molecules membrane activity membrane structure monoclonal antibody natural killer cells neoplasm /cancer immunology phagocytes protein biosynthesis protein structure surface antigens tissue /cell culture
项目摘要
Natural killer (NK) cells, cytotoxic T-lymphocytes (CTL's), and
mononuclear phagocytes (MP) represent three major systems of
host defense against tumors. Our laboratory is actively involved
in the molecular dissection of cell-surface events important in the
cytotoxic response mediated by these cells, through the use of
monoclonal antibodies as probes of structure and function. In this
project, we propose to continue our studies examining the role of
the Lymphocyte Function-Associated Antigen-One (LFA-1)
heterodimeric family of surface glycoproteins on cytotoxic cells,
with special emphasis on the NK system and a closely-related
effector cell, Lymphokine (IL-2)-Activated Killer Cells.
Our laboratory is currently exploring the following hypotheses in
cytotoxic systems: (1) that cell surface density of LFA-1 family
members is important in expression of cell-mediated cytotoxicity
in these systems; (2) that LFA-1 subserves non-adherence related
function(s) in the NK system, possibly playing a role in a late step
in the cytolytic mechanism or in more global regulation of
cellular processes (e.g., transmembrane signalling events); and (3)
that one important effect of IL-2 in modulating cytolytic activity
is in enhancing expression of LFA-1, through as yet unknown
mechanisms. In this Competing Continuation Application, we
propose a series of experiments designed to further test these
hypotheses through detailed study of the structure, function,
expression, and biosynthesis of this important family of surface
molecules, as well as proposals to attempt to isolate and identify
the putative target cell ligand for LFA-1 in the NK system. In so
doing, we will continue to pursue our long-term goal of better
understanding, at the molecular level, cell-mediated host defense
against tumors.
自然杀伤细胞(NK),细胞毒性t淋巴细胞(CTL),以及
项目成果
期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Differentiation-inducing cytokine P48 exists in a membrane-associated form.
分化诱导细胞因子 P48 以膜相关形式存在。
- DOI:
- 发表时间:1991
- 期刊:
- 影响因子:0
- 作者:Kostyal,DA;Beezhold,DH;Hall,RE
- 通讯作者:Hall,RE
Resistance to natural killer cell-mediated cytolysis by a pleiotropic drug-resistant human erythroleukemia (K562-R) cell line.
多效耐药人红白血病 (K562-R) 细胞系对自然杀伤细胞介导的细胞溶解的抵抗。
- DOI:
- 发表时间:1986
- 期刊:
- 影响因子:11.2
- 作者:Yanovich,S;Hall,RE;Weinert,C
- 通讯作者:Weinert,C
Interleukin-2 modulates the expression of lymphocyte function-associated antigen-one (LFA-1) and p150,95 during the generation of lymphokine-activated killer (LAK) cells.
Interleukin-2 在淋巴因子激活杀伤 (LAK) 细胞生成过程中调节淋巴细胞功能相关抗原一 (LFA-1) 和 p150,95 的表达。
- DOI:
- 发表时间:1989
- 期刊:
- 影响因子:6.4
- 作者:Grant,AJ;Merchant,RE;Hall,RE
- 通讯作者:Hall,RE
Transient inhibition of DNA synthesis by 5-fluorodeoxyuridine leads to overexpression of dihydrofolate reductase with increased frequency of methotrexate resistance.
5-氟脱氧尿苷短暂抑制 DNA 合成会导致二氢叶酸还原酶过度表达,从而增加甲氨蝶呤耐药频率。
- DOI:
- 发表时间:1988
- 期刊:
- 影响因子:0
- 作者:Schuetz,JD;Gorse,KM;Goldman,ID;Westin,EH
- 通讯作者:Westin,EH
Human p150,95 alpha-subunit: genomic organization and analysis of the 5'-flanking region.
人类 p150,95 α 亚基:基因组组织和 5 侧翼区域分析。
- DOI:10.1089/dna.1992.11.123
- 发表时间:1992
- 期刊:
- 影响因子:3.1
- 作者:Noti,JD;Gordon,M;Hall,RE
- 通讯作者:Hall,RE
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ROBERT E HALL其他文献
ROBERT E HALL的其他文献
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{{ truncateString('ROBERT E HALL', 18)}}的其他基金
CYTOKINE INDUCTION BY A 48 KD MYCOPLASMA GENE PRODUCT
48 KD 支原体基因产物诱导细胞因子
- 批准号:
2748893 - 财政年份:1997
- 资助金额:
$ 16.28万 - 项目类别:
CYTOKINE INDUCTION BY A 48 KD MYCOPLASMA GENE PRODUCT
48 KD 支原体基因产物诱导细胞因子
- 批准号:
2895749 - 财政年份:1997
- 资助金额:
$ 16.28万 - 项目类别:
CYTOKINE INDUCTION BY A 48 KD MYCOPLASMA GENE PRODUCT
48 KD 支原体基因产物诱导细胞因子
- 批准号:
2393449 - 财政年份:1997
- 资助金额:
$ 16.28万 - 项目类别:
CYTOKINE INDUCTION BY A 48 KD MYCOPLASMA GENE PRODUCT
48 KD 支原体基因产物诱导细胞因子
- 批准号:
6555584 - 财政年份:1997
- 资助金额:
$ 16.28万 - 项目类别:
TUMOR CELL MEMBRANE MOLECULE INDUCTION OF MONOCYTE TNF
单核细胞TNF的肿瘤细胞膜分子诱导
- 批准号:
2098911 - 财政年份:1992
- 资助金额:
$ 16.28万 - 项目类别:
TUMOR CELL MEMBRANE MOLECULE INDUCTION OF MONOCYTE TNF
单核细胞TNF的肿瘤细胞膜分子诱导
- 批准号:
3202428 - 财政年份:1992
- 资助金额:
$ 16.28万 - 项目类别:
TUMOR CELL MEMBRANE MOLECULE INDUCTION OF MONOCYTE TNF
单核细胞TNF的肿瘤细胞膜分子诱导
- 批准号:
3202429 - 财政年份:1992
- 资助金额:
$ 16.28万 - 项目类别:
KILLER CELL SURFACE ANTIGENS--BIOCHEMISTRY AND FUNCTION
杀伤细胞表面抗原——生物化学和功能
- 批准号:
3174699 - 财政年份:1987
- 资助金额:
$ 16.28万 - 项目类别:
KILLER CELL SURFACE ANTIGENS: BIOCHEMISTRY AND FUNCTION
杀伤细胞表面抗原:生物化学和功能
- 批准号:
3174707 - 财政年份:1987
- 资助金额:
$ 16.28万 - 项目类别:
KILLER CELL SURFACE ANTIGENS--BIOCHEMISTRY AND FUNCTION
杀伤细胞表面抗原——生物化学和功能
- 批准号:
3174705 - 财政年份:1987
- 资助金额:
$ 16.28万 - 项目类别: