Interleukin-18 inhibits human immunodeficiency virus type 1 production in peripheral blood mononuclear cells
Interleukin-18 inhibits human immunodeficiency virus type 1 production in peripheral blood mononuclear cells
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DOI：
10.1086/322805
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发表时间：
2001-09-01
影响因子：
6.4
通讯作者：
Shapiro, L
中科院分区：
文献类型：
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作者：
Choi, HJ;Dinarello, CA;Shapiro, L
白细胞介素（IL）-18是干扰素（IFN）-γ诱导因子，并有助于Th 1免疫应答。IL-18与单核细胞嗜性人类免疫缺陷病毒1型（HIV-1）感染后加入外周血单个核细胞（PBMC）抑制p24抗原的产生最多72%。这些培养物中IFN-γ水平增加，并且观察到HIV-1产生与IFN-γ水平之间的显著负相关。中和性抗IFN-γ抗体逆转了IL-18的抑制作用。在感染前用IL-18预孵育PBMC抑制p24，而无需额外的IL-18（64%）。然而，与4天培养后观察到的IL-18抑制程度相比，在第5-13天期间未观察到额外的IL-18抑制作用。IL-18还降低了HIV-1受体CD 4的细胞表面表达。这些结果表明，IL-18通过中间体IFN-γ抑制PBMC中的HIV-1产生。此外，在病毒感染的早期阶段存在抑制作用，并与HIV-1受体表达减少有关。
Interleukin (IL)-18 is an interferon (IFN)-gamma -inducing factor and contributes to the Th1 immune response. IL-18 added after infection of peripheral blood mononuclear cells (PBMC) with monocyte-tropic human immunodeficiency virus type 1 (HIV-1) inhibited p24 antigen production by a maximum of 72%. IFN-gamma levels in these cultures were increased, and a significant inverse relationship between HIV-1 production and IFN-gamma levels was observed. A neutralizing anti-IFN-gamma antibody reversed the IL-18 inhibitory effect. Preincubation of PBMC with IL-18 before infection inhibited p24 without additional IL-18 (64%). However, compared with the degree of IL-18 inhibition observed after a 4-day culture, no additional IL-18 inhibitory effect was observed during days 5-13. IL-18 also reduced cell surface expression of the HIV-1 receptor CD4. These results demonstrate that IL-18 inhibited HIV-1 production in PBMC through intermediate IFN-gamma. Furthermore, inhibition was present during the early stages of viral infection and was associated with reduced HIV-1 receptor expression.