人疱疹病毒6型诱导单核细胞产生IL-10

Human herpesvirus-6 infection induces IL-10 production in monocytes

目的探讨人疱疹病毒６型（ＨＨＶ－６）感染的免疫发病机理。方法用逆转录－聚合酶链反应（ＲＴ－ＰＣＲ）和双抗体夹心酶联免疫吸附试验（ＥＬＩＳＡ）检测白细胞介素－１０（ＩＬ－１０）等细胞因子的产生。结果ＨＨＶ－６诱导单核细胞表达和产生ＩＬ－１０，细胞因子ｍＲＮＡ动力学研究发现ＴＮＦ－α（肿瘤坏死因子）、ＩＬ－１β及ＩＬ－６随ＩＬ－１０ｍＲＮＡ积累而减少，用抗人ＩＬ－１０单克隆抗体阻断ＨＨＶ－６诱导的内源性ＩＬ－１０，ＴＮＦ－α、ＩＬ－１β和ＩＬ－６ｍＲＮＡ的表达和因子产生明显增加，表明ＨＨＶ－６诱导的内源性ＩＬ－１０在转录水平能抑制单核细胞因子产生。结论ＩＬ－１０具有抑制Ｉ类辅助性Ｔ细胞（Ｔｈ１）反应、下调单核巨噬细胞功能等多种生物作用，推测ＨＨＶ－６诱导产生的内源性ＩＬ－１０与该病毒长期潜伏感染及其参予的免疫功能紊乱有关。

In this report,interleukin 10(IL-10)and other cytokines were evaluated through reverse transcription-polymerase chain raction (RT-PCR)and sandwich ELISA to explore possible immune pathogenesis of human herpesvirus 6 (HHV-6) infection.The results showed that IL-10 was expressed in HHV-6 infected monocytes.Kinetic studies found that transcription of IL-1β,IL-6 and TNF-α mRNA decreased with accumulation of IL-10 mRNA.When endogenous IL-10 induced by HHV-6 was blocked using anti-human IL-10 monoclonal antibody,the production and the expression of TNF-α,IL-1βand IL-6 markedly increased as compared with infection by HHV-6 alone,indicating that endogenous IL-10 inhibited cytokine production at the transcription level in HHV-6 infected monocytes.IL-10 has been shown to suppress Th1 response and down-regulate monocyte/macrophage function.The data from our studies suggest that disturbance of immune function and latent infection resulting from HHV-6 infection might partially contribute to endogenous IL-10 production.