Study on growth and differentiation of human eosinophils
人嗜酸性粒细胞生长和分化的研究
基本信息
- 批准号:62570532
- 负责人:
- 金额:$ 1.15万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1987
- 资助国家:日本
- 起止时间:1987 至 1988
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Human eosinophilic cell line EoL-1 was studied by using luminol-dependent chemiluminescence for respiratory burst upon stimulation with phorbol ester (TPA) and N-formylpeptide (fMLP). Treatment of EoL-1 with interferon- (IFN- ) for 5 days strongly enhanced TPA-inducible CL response. IFN- A had a similar effect. Tumor necrosis factor (TNF) also enhanced TPAinducible CL response of EOL-1 and, furthermore, was quite inhiditory to EoL-1 cell growth. On the other hand, interleukin 5 (IL-5) or granulocyte-macrophage colony stimulating factor (GM-CSF) had no augmenting effect on TPA-inducible CL in EoL-1. IL-5, however, slightly enhanced the effect of IFN- . Furthermore, both IL-5 and GM-CSF showed slight growth-promoting effects on EoL-1. EoL-1 pretreated with IFN- , - A or TNf also became capable of producing CL response to fMLP, and IFN- and TNF were again synergistic.EoL-1 treated with IFN- , - A, or TNF had abundant cytoplasm, but only TNF increased cells having distinct eosinophilic granules. IFN- enhanced this cytological effect of TNF. It was further demonstrated that the simultaneous treatment of EoL-1 with IFN- and TNF strongly increased the binding sites for phorbol diesters and also dramatically induced the surface expression of fMLP receptors. Taken together, EoL-1 seems to provide a valuable experimental model for the study of the ontogeny and the function of human eosinophils and as a source of their products.
用佛波酯(TPA)和N-甲酰肽(fMLP)刺激人嗜酸性粒细胞系EoL-1,用鲁米诺依赖的化学发光法研究其呼吸爆发。用干扰素-(IFN-)处理EoL-1 5天强烈增强TPA诱导的CL应答。IFN-α也有类似的作用。肿瘤坏死因子(TNF)也能增强TPA诱导的EoL-1细胞的CL反应,并对EoL-1细胞的生长有明显的抑制作用。另一方面,白细胞介素5(IL-5)或粒细胞-巨噬细胞集落刺激因子(GM-CSF)对EoL-1中TPA诱导的CL没有增强作用。而IL-5对IFN-γ的作用稍有增强。此外,IL-5和GM-CSF均对EoL-1显示轻微的生长促进作用。用IFN-α、-A或TNF预处理的EoL-1也能产生对fMLP的CL反应,IFN-α和TNF又有协同作用。IFN-γ增强了TNF的这种细胞学效应。进一步证明,用IFN-γ和TNF同时处理EoL-1强烈增加了佛波醇二酯的结合位点,并且还显著诱导了fMLP受体的表面表达。两者合计,EoL-1似乎提供了一个有价值的实验模型的个体发育和人类嗜酸性粒细胞的功能的研究,并作为其产品的来源。
项目成果
期刊论文数量(3)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Osamu,Yoshie: Journal of Leukocyte Biology. 45. 10-20 (1989)
Osamu,Yoshie:白细胞生物学杂志。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Osamu Yoshie.: Journal of Leukocyte Biology. 45. 10-20 (1989)
Osamu Yoshie.:白细胞生物学杂志。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
YOSHIE Osamu其他文献
A CC3 variant of lymphotactin/XCL1 (XCL1-CC3) functions as a potent adjuvant to accumulate CD103+XCR1+ cross-presenting dendritic cells and induce antigen-specific CD8+ T cell responses
淋巴趋化素/XCL1 (XCL1-CC3) 的 CC3 变体可作为有效佐剂积聚 CD103 XCR1 交叉呈递树突状细胞并诱导抗原特异性 CD8 T 细胞应答
- DOI:
- 发表时间:
2016 - 期刊:
- 影响因子:0
- 作者:
YAMAMOTO Shinya;MATSUO Kazuhiko;YOSHIE Osamu;NAKAYAMA Takashi - 通讯作者:
NAKAYAMA Takashi
YOSHIE Osamu的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('YOSHIE Osamu', 18)}}的其他基金
Learning support mechanism based on analysis of consensus building among users
基于用户共识分析的学习支持机制
- 批准号:
15K00495 - 财政年份:2015
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Role of CCL28 for mucosal immunity
CCL28 对粘膜免疫的作用
- 批准号:
26460582 - 财政年份:2014
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Transcriptional regulation of CCR7 expression in mature T-cell malignancies
成熟 T 细胞恶性肿瘤中 CCR7 表达的转录调控
- 批准号:
23501273 - 财政年份:2011
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Study on the pathophysiological role of the Th2-type chemokine receptor CCR4
Th2型趋化因子受体CCR4的病理生理作用研究
- 批准号:
19390277 - 财政年份:2007
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Transcriptional regulation of CCR10 expression in plasma cells
浆细胞中 CCR10 表达的转录调控
- 批准号:
17590443 - 财政年份:2005
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Elucidation of Pathoptysiological Roles of Immune Chemokines
免疫趋化因子病理学作用的阐明
- 批准号:
11470091 - 财政年份:1999
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
相似海外基金
The contribution of respiratory burst to antibiotic failure in Staphylococcus aureus bacteremia
呼吸爆发对金黄色葡萄球菌菌血症抗生素失效的影响
- 批准号:
10666777 - 财政年份:2022
- 资助金额:
$ 1.15万 - 项目类别:
Respiratory burst activity of ayu (Plecoglossus altivelis) neutrophils : comparison with other fresh water fish
香鱼(Plecoglossus altivelis)中性粒细胞的呼吸爆发活动:与其他淡水鱼的比较
- 批准号:
15580173 - 财政年份:2003
- 资助金额:
$ 1.15万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
MONOCYTE PATHOGENESIS--RESPIRATORY BURST OXIDASE
单核细胞发病机制--呼吸爆发氧化酶
- 批准号:
6527587 - 财政年份:1999
- 资助金额:
$ 1.15万 - 项目类别:
MONOCYTE PATHOGENESIS--RESPIRATORY BURST OXIDASE
单核细胞发病机制--呼吸爆发氧化酶
- 批准号:
2766775 - 财政年份:1999
- 资助金额:
$ 1.15万 - 项目类别:
MONOCYTE PATHOGENESIS--RESPIRATORY BURST OXIDASE
单核细胞发病机制--呼吸爆发氧化酶
- 批准号:
6390222 - 财政年份:1999
- 资助金额:
$ 1.15万 - 项目类别:
MONOCYTE PATHOGENESIS--RESPIRATORY BURST OXIDASE
单核细胞发病机制--呼吸爆发氧化酶
- 批准号:
6184578 - 财政年份:1999
- 资助金额:
$ 1.15万 - 项目类别:
RESPIRATORY BURST, CYTOKINES AND HIV IN ALCOHOLICS
酗酒者的呼吸爆发、细胞因子和 HIV
- 批准号:
2516830 - 财政年份:1996
- 资助金额:
$ 1.15万 - 项目类别:
RESPIRATORY BURST, CYTOKINES AND HIV IN ALCOHOLICS
酗酒者的呼吸爆发、细胞因子和 HIV
- 批准号:
2769166 - 财政年份:1996
- 资助金额:
$ 1.15万 - 项目类别:
RESPIRATORY BURST, CYTOKINES AND HIV IN ALCOHOLICS
酗酒者的呼吸爆发、细胞因子和 HIV
- 批准号:
2047399 - 财政年份:1996
- 资助金额:
$ 1.15万 - 项目类别:
NADPH-BINDING PROTEIN OF THE RESPIRATORY BURST OXIDASE
呼吸爆发氧化酶的 NADPH 结合蛋白
- 批准号:
3145787 - 财政年份:1991
- 资助金额:
$ 1.15万 - 项目类别: