Yu H S, Chang K L, Yu C L, Wu C S, Chen G S, Ho J C
Department of Dermatology, Kaohsiung Medical College, Taiwan, Republic of China.
Arch Dermatol Res. 1998 Dec;290(12):681-7. doi: 10.1007/s004030050373.
The immune function of peripheral mononuclear cells (MNC) in patients with endemic arsenic-induced Bowen's disease (BD) was investigated. Many cytokines and immune-related factors were determined in the present study. Interleukin-1beta and TNF-alpha production was used as an indicator of monocyte/macrophage function. II-2 and sIL-2R production was used as an indicator of lymphocyte activation. The release of sCD4 and sCD8 was used as an indicator of activation of respective T-cell subpopulations. Production of IFN-gamma and IL-2 reflected the cellular effector function of helper T-cells type 1. In vivo cell-mediated immunity was also assessed by estimation of the percentage of T-cells in peripheral blood MNC and the nonspecific delayed-type hypersensitivity (DTH) response to 2,4-dinitrochlorobenzene (DNCB). Both assays revealed depressed cell-mediated immunity in BD. Compared with healthy controls, spontaneous and PHA-induced IFN-gamma and TNF-alpha production was significantly decreased in BD whereas spontaneous release of IL-2, sCD4 and sCD8 was significantly increased. Although PHA stimulation increased IL-2 release, the expression of IL-2R alpha and beta chains and the release of sIL-2R were not proportionately increased in BD. In addition, IL-2-mediated [3H]-thymidine incorporation by MNC in patients with BD was significantly decreased. These findings suggest that the defective cell-mediated immune function in BD is due to impairment of membrane IL-2R expression in lymphocytes after stimulation.
对地方性砷中毒所致鲍温病（BD）患者外周血单个核细胞（MNC）的免疫功能进行了研究。本研究测定了多种细胞因子和免疫相关因子。白细胞介素-1β和肿瘤坏死因子-α的产生用作单核细胞/巨噬细胞功能的指标。II-2和可溶性白细胞介素-2受体（sIL-2R）的产生用作淋巴细胞活化的指标。可溶性CD4和可溶性CD8的释放用作各T细胞亚群活化的指标。γ干扰素（IFN-γ）和白细胞介素-2的产生反映了1型辅助性T细胞的细胞效应功能。还通过估计外周血MNC中T细胞的百分比以及对2,4-二硝基氯苯（DNCB）的非特异性迟发型超敏反应（DTH）来评估体内细胞介导的免疫。这两种检测均显示BD患者的细胞介导免疫功能低下。与健康对照相比，BD患者自发和PHA诱导的IFN-γ和肿瘤坏死因子-α产生显著降低，而IL-2、可溶性CD4和可溶性CD8的自发释放显著增加。尽管PHA刺激增加了IL-2的释放，但BD患者中IL-2Rα和β链的表达以及sIL-2R的释放并未相应增加。此外，BD患者中MNC的IL-2介导的[3H]-胸腺嘧啶核苷掺入显著降低。这些发现表明，BD患者细胞介导免疫功能缺陷是由于刺激后淋巴细胞中膜IL-2R表达受损所致。
