N-acetylcysteine attenuates TNF-alpha-dependent reduction of IL-4-induced Fc(epsilon)RII expression in human monocytes

作者：Hashimoto S^*; Gon Y; Nakayama T; Yoshida S; Hayashi S; Maruoka S; Yodoi J; Horie T

来源：Allergy, 1997, 52(9): 909-913.

DOI：10.1111/j.1398-9995.1997.tb01250.x

• FC epsilon RII
• monocyte
• N-acetylcysteine

We have previously shown that tumor necrosis factor-alpha (TNF-alpha) reduces interleukin-4 (IL-4)-induced Fc(epsilon)RII expression in human monocytes. It has been shown that TNF-alpha activates nuclear transcriptional factors through the generation of reactive oxygen intermediates (ROIs), and antioxidant N-acetylcysteine (NAC) inhibits TNF-alpha-induced activation of nuclear transcriptional factors. Therefore, we hypothesized that TNF-alpha-dependent reduction of IL-4-induced Fc(epsilon)RII expression in monocytes might be mediated through the ROIs-activated mechanism. In the present study, to test our hypothesis, we examined the effect of NAC on TNF-alpha-dependent reduction of IL-4-induced Fc(epsilon)RII expression in human monocytes. NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc(epsilon)RII expression by attenuating TNF-alpha-dependent reduction of Fc(epsilon)RII mRNA expression. Similarly, the structurally unrelated antioxidant, pyrrolidine dithiocarbamate (PDTC), also effectively attenuated this reduction. These results indicate that an ROIs-activated and antioxidant-sensitive mechanism might be involved in TNF-alpha-dependent reduction of IL-4-induced Fc(epsilon)RII expression in monocytes.

• 出版日期1997-9