The type B receptor for tumor necrosis factor-alpha mediates DNA fragmentation in HL-60 and U937 cells and differentiation in HL-60 cells.
The type B receptor for tumor necrosis factor-alpha mediates DNA fragmentation in HL-60 and U937 cells and differentiation in HL-60 cells.
复制标题
肿瘤坏死因子-α 的 B 型受体介导 HL-60 和 U937 细胞中的 DNA 断裂以及 HL-60 细胞中的分化。
作者：
M. Greenblatt;L. Elias
肿瘤坏死因子-α（TNF）与HL-60和U937细胞上的两种特异性细胞表面受体A和B结合，诱导HL-60细胞向单核细胞样分化，并诱导HL-60和U937细胞早期DNA断裂。为了进一步确定受体的作用，我们研究了针对每个受体的单克隆抗体（MoAb）如何影响TNF诱导的细胞反应。HTR-9是一种抗B型（低亲和力，55 Kd）受体的单克隆抗体，以剂量依赖性方式再现了所有这些作用。UTR-1是一种抗A型受体（高亲和力，75 Kd）的单克隆抗体，在饱和剂量下没有效果，但过饱和剂量使DNA片段化增强三倍。TNF和干扰素-γ（IFN-γ）协同诱导形态分化和单核细胞抗原表达，而抗B受体单克隆抗体是协同的形态反应，但不是抗原表达。我们的研究结果表明：（1）B型受体介导HL-60和U937细胞对TNF的某些反应，（2）A型受体不刺激这些反应，（3）TNF分子不是这些反应所必需的，（4）TNF诱导的HL-60细胞形态学变化和表面抗原表达可能受不同的受体后途径调节。
Tumor necrosis factor-alpha (TNF) binds to two specific cell surface receptors, types A and B, which are both present on HL-60 and U937 cells, and induces monocytoid differentiation in HL-60 cells and early DNA fragmentation in HL-60 and U937 cells. To further define the receptors' roles, we studied how monoclonal antibodies (MoAbs) against each receptor affected TNF-induced cellular responses. HTR-9, an MoAb against the type B (low affinity, 55 Kd) receptor, reproduced all of these effects in a dose-dependent manner. UTR-1, an MoAb against the type A (high affinity, 75 Kd) receptor, had no effect in saturating doses, but supersaturating doses enhanced DNA fragmentation threefold. TNF and interferon gamma (IFN-gamma) synergistically induced morphologic differentiation and monocytic antigen expression, while the antitype B receptor MoAb was synergistic for morphologic response, but not antigen expression. Our results indicate that (1) the type B receptor mediates some responses to TNF in HL-60 and U937 cells, (2) the type A receptor does not stimulate these responses, (3) the TNF molecule is not necessary for some of these actions, and (4) TNF-induced morphologic changes and surface antigen expression in HL-60 cells may be regulated by separate postreceptor pathways.
影响因子：
3.9
作者：
Pal, Nabanita;Kim, Taeyeon;Park, Jae-Seo;Cho, Eun-Bum
通讯作者：
Cho, Eun-Bum
肿瘤坏死因子受体介导的人早幼粒细胞单核细胞分化：与干扰素-γ和 1,25-二羟基维生素 D3 的协同作用。
影响因子：
20.3
作者：
Weinberg,JB;Larrick,JW
通讯作者：
Larrick,JW
肿瘤坏死因子-α 1 细胞内作用的直接证据。显微注射肿瘤坏死因子可杀死靶细胞。
DOI：
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发表时间：
1990
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Smith,MR;Munger,WE;Kung,HF;Takacs,L;Durum,SK
通讯作者：
Durum,SK