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白细胞介素-4对细胞因子诱导的原单核细胞U1细胞中HIV1和白细胞介素-8表达的调节作用具有浓度依赖性和细胞因子依赖性。

Interleukin-4 regulation of cytokine-induced HIV1 and interleukin-8 expression in promonocytic U1 cells is concentration- and cytokine-dependent.

作者信息

Tiemessen C T, Kilroe B, Martin D J

机构信息

MRC AIDS Virus Research Unit, National Institute for Virology, University of the Witwatersrand, Johannesburg, South Africa.

出版信息

Res Virol. 1998 Jan-Feb;149(1):21-7. doi: 10.1016/s0923-2516(97)86897-5.

Abstract

IL4 has been shown to differentially modulate HIV1 replication in primary cells of the monocyte/macrophage lineage. Its effects on chronic HIV1 infection, however, are unknown. To address IL4-mediated effects on promonocytic cells chronically infected with HIV1, U1 cells were incubated in the presence or absence of IL4 together with cytokines that are known to induce both HIV1 and IL8 expression. IL4 enhanced IL1 beta-induced HIV1 and IL8 expression in promonocytic U1 cells, whereas it suppressed their expression induced by cytokines IL6, GM-CSF and to a small extent, TNF alpha. IL4 suppressed IFN gamma-induced IL8 production with increasing IL4 concentration, while HIV1 p24 core antigen production was suppressed at low IL4 input (0.1 and 1 U/ml) but was substantially enhanced at a high IL4 input concentration (10 U/ml). Results showed that the immunosuppressive cytokine IL4 can behave variably in modulating HIV1 and IL8 expression, depending on both the inducing cytokine and the input concentration of IL4.

摘要

白细胞介素4(IL4)已被证明可不同程度地调节单核细胞/巨噬细胞谱系原代细胞中的HIV-1复制。然而,其对慢性HIV-1感染的影响尚不清楚。为了研究IL4对慢性感染HIV-1的前单核细胞的作用,将U1细胞在有或无IL4的情况下与已知可诱导HIV-1和IL8表达的细胞因子一起孵育。IL4增强了IL-1β诱导的前单核细胞U1细胞中HIV-1和IL8的表达,而抑制了细胞因子IL-6、粒细胞-巨噬细胞集落刺激因子(GM-CSF)以及在一定程度上肿瘤坏死因子α(TNFα)诱导的它们的表达。随着IL4浓度的增加,IL4抑制了干扰素γ(IFNγ)诱导的IL8产生,而HIV-1 p24核心抗原的产生在低IL4输入量(0.1和1 U/ml)时受到抑制,但在高IL4输入浓度(10 U/ml)时显著增强。结果表明,免疫抑制细胞因子IL4在调节HIV-1和IL8表达方面表现各异,这取决于诱导细胞因子和IL4的输入浓度。

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