Slow release of soluble TNF receptors by monocytes in vitro.
Slow release of soluble TNF receptors by monocytes in vitro.
复制标题
DOI：
10.4049/jimmunol.152.8.4036
复制
发表时间：
1994-04
影响因子：
4.4
通讯作者：
J. Leeuwenberg;T. Jeunhomme;W. Buurman
中科院分区：
文献类型：
--
作者：
J. Leeuwenberg;T. Jeunhomme;W. Buurman
在本研究中，我们研究了可溶性TNF-R在PBMC体外的释放。单抗cd3激活T细胞，以及phorbol酯（PMA）激活，增强了PBMC对sTNF-R55和sTNF-R75的释放。与中性粒细胞激活后释放TNF-R相比，PBMC释放sTNF-R是一个相对缓慢的过程，培养2天后达到平台期。单核细胞似乎是释放sTNF-R的主要来源，而与整个细胞群相比，纯化T细胞的激活仅诱导少量sTNF-R释放。为了揭示这一机制，在2天的细胞培养过程中加入了一些细胞因子。IL-10增强sTNF-R水平的动力学与mAb抗cd3和PMA相似，而其他细胞因子不影响PBMC、纯T淋巴细胞或纯化单核细胞（激活或未激活）释放sTNF-R。相反，在激活期加入细胞因子抑制剂，研究内源性细胞因子对sTNF-R释放的影响。抗il -10和IL-1ra单克隆抗体部分释放sTNF-R，而其他抑制剂不影响释放。在体外获得的结果可以扩展我们对体内炎症反应中sTNF-R增强的机制的了解。
In this study, we investigated the release of soluble(s) TNF-R by PBMC in vitro. T cell activation by mAb anti-CD3, as well as activation with phorbol esters (PMA), enhanced the release of both sTNF-R55 and sTNF-R75 by PBMC. In contrast to shedding of TNF-R by neutrophils upon activation, release of sTNF-R by PBMC proved to be a relatively slow process, reaching a plateau after 2 days of culture. Monocytes appeared to be the main source of the released sTNF-R, whereas activation of purified T cells induced only a minor release of sTNF-R as compared with the whole cell population. To unravel the mechanism, a number of cytokines were added during a 2-day culture of cells. IL-10 enhanced sTNF-R levels with similar kinetics as mAb anti-CD3 and PMA, whereas the other cytokines tested did not affect the release of sTNF-R by PBMC, pure T lymphocytes, or purified monocytes, either activated or not. Conversely, inhibitors of cytokines were added during the activation period to study the effect of endogenously produced cytokines on sTNF-R release. mAb anti-IL-10 and IL-1ra partly sTNF-R release, whereas other inhibitors did not affect the release. The results obtained in vitro may extend our insight in the mechanism via which sTNF-R are enhanced in vivo during inflammatory reactions.