IL-10 and IL-4 synergize with TNF-alpha to induce IL-1ra production by human neutrophils
IL-10 and IL-4 synergize with TNF-alpha to induce IL-1ra production by human neutrophils
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DOI：
10.1006/cyto.1996.0021
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发表时间：
1996-02-01
期刊：
影响因子：
3.8
通讯作者：
Cavaillon, JM
中科院分区：
文献类型：
--
作者：
Marie, C;Pitton, C;Cavaillon, JM
IL-4、IL-10、IL-13和TGF-β的抗炎特性与它们抑制促炎细胞因子的产生和促进白细胞介素-1受体拮抗剂（IL-1 ra）释放的能力相关。在这里，我们研究了它们对活化的人多形核细胞（PMN）的作用，IL-4和TGF-β能够增加IL-1 ra的产生，然而，在LPS存在下，只有IL-4能够进一步增加IL-1 ra的产生。当TNF-α诱导PMN产生IL-1 ra时，总之，IL-10本身不能诱导IL-1 ra，也不能放大LPS诱导的PMN产生IL-1 ra，但当TNF-α是触发信号时，IL-4在测试的不同组合中具有活性; IL-13和TGF-β没有进一步调节LPS和TNF-α诱导的PMN产生IL-1 ra。(C)1996年学术出版社
The anti-inflammatory properties of IL-4, IL-10, IL-13 and TGF-beta are associated with their ability to repress the production of pro-inflammatory cytokines and to favour the release of interleukin-1 receptor antagonist (IL-1ra). Here, we investigate their actions on activated human polymorphonuclear cells (PMN), IL-4 and TGF-beta were able to increase the production of IL-1ra, however only IL-4 were able to further increase IL-1ra production in the presence of LPS. When IL-1ra production by PMN was induced by tumour necrosis factor-alpha (TNF-alpha), IL-10 and IL-4 both amplified its release and its presence as a cell-associated form, In conclusion, IL-10 which was unable to induce IL-1ra by itself or to amplify the LPS-induced production by PMN, was able to increase its release when TNF-alpha, is the triggering signal, IL-4 was active in the different combinations tested; IL-13 and TGF-beta did not further modulate LPS- and TNF-alpha-induced IL-1ra production by PMN. (C) 1996 Academic Press Limited