IL-4-independent regulation of in vivo IL-9 expression.

IL-4-independent regulation of in vivo IL-9 expression.
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DOI:
10.4049/jimmunol.159.6.2616
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发表时间:
1997-09
影响因子:
4.4
通讯作者:
P. Monteyne;J. Renauld;J. van Broeck;D. Dunne;F. Brombacher;J. Coutelier
P. Monteyne;J. Renauld;J. van Broeck;D. Dunne;F. Brombacher;J. Coutelier
中科院分区:
医学2区
文献类型:
--
作者:
P. Monteyne;J. Renauld;J. van Broeck;D. Dunne;F. Brombacher;J. Coutelier

文献摘要

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我们重点研究了IL-4在Th2细胞因子IL-9调节中的作用。在体内,可溶性AGS免疫后的小鼠淋巴结中可检测到IL-9mRNA。IL-9的表达先于IL-4,在IL-4基因敲除的小鼠中不受影响。相反,在IL-10缺陷的小鼠中观察到IL-9消息的显著减少,这表明该细胞因子在诱导IL-9产生中起作用。抗CD4抗体处理和纯化的CD4细胞分析证实,IL-9是由CD4+细胞产生的。此外,与已报道的IL-4类似,感染乳酸脱氢酶提升病毒后,IL-9消息诱导显著降低。用抗CD3单抗刺激后,检测IL-9mRNA的表达。在该模型中,IL-9的表达与IL-4的表达一致,但在IL-4缺陷的小鼠中没有减少。这与体外刺激不同,在体外刺激中,与抗CD3抗体和共刺激分子孵育的淋巴细胞中IL-9的表达似乎是一种晚期事件,部分依赖于IL-4。在体外,加入抗IL-4单抗后,IL-9的分泌显著减少,IL-4基因缺陷小鼠的淋巴细胞中IL-9的分泌也显著减少。综上所述,我们的结果表明,Th2细胞因子IL-9可以通过IL-4依赖和非依赖途径表达。
We focused on the role of IL-4 in the regulation of the Th2 cytokine IL-9. In vivo, IL-9 mRNA was detected in lymph nodes after immunization with soluble Ags. IL-9 expression preceded that of IL-4, and was not affected in IL-4 knockout mice. In contrast, a significant decrease of IL-9 message was observed in IL-10-deficient mice, indicating a role for this cytokine in the induction of IL-9 production. Treatment with anti-CD4 Ab and analysis of purified CD4 cells confirmed that IL-9 was produced by CD4+ cells. Moreover, similarly to what has been reported for IL-4, IL-9 message induction was strongly decreased by infection with lactate dehydrogenase-elevating virus. IL-9 mRNA was also detected after in vivo stimulation with anti-CD3 Ab. In this model, IL-9 expression followed that of IL-4, but was not reduced in IL-4-deficient mice. This contrasts with in vitro stimulation in which, as reported in humans, IL-9 expression in lymphocytes incubated with anti-CD3 Ab and costimulatory molecules appeared as a late event, and was partly dependent on IL-4. In vitro IL-9 secretion was reduced significantly by addition of anti-IL-4 Ab, as well as in lymphocytes from IL-4 gene-deficient mice. Taken together, our results indicate that the Th2 cytokine IL-9 can be expressed by both IL-4-dependent and -independent pathways.