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I型人嗜T淋巴细胞病毒携带者中γ干扰素产量增加,但白细胞介素4产量未增加。

Increased production of interferon gamma but not interleukin 4 in human T-lymphotropic virus type I carriers.

作者信息

Shimamoto Y, Funai N, Watanabe M, Suga K

机构信息

Department of Internal Medicine, Saga Medical School, Japan.

出版信息

Int J Hematol. 1996 Aug;64(2):111-8. doi: 10.1016/0925-5710(96)00472-0.

DOI:10.1016/0925-5710(96)00472-0
PMID:8854568
Abstract

We investigated the production of interferon gamma (IFN-gamma), interleukin 4 (IL-4), IL-1 alpha, and tumor necrosis factor alpha (TNF-alpha) by peripheral blood mononuclear cells (PBMCs) from human T-lymphotropic virus type I(HTLV-I) carriers during short-term in vitro culture, in comparison with that by those from HTLV-I seronegative controls. PBMCs isolated from eight carriers and eight controls were cultured, and cytokine levels were measured in 1- and 3-day culture supernatants. Enhanced production of IFN-gamma was observed in all HTLV-I carriers but none of the controls. IL-4 production was not increased in the carriers except for one with a past history of toxoplasma lymphadenitis. IL-1 alpha and TNF-alpha levels were higher in the carriers. CD4+ cells were responsible for the enhanced IFN-gamma production, while monocytes were responsible for the increased IL-1 alpha and TNF-alpha production. The present study showed that the PBMCs from HTLV-I carriers consistently produced large amounts of some cytokines (IFN-gamma, IL-1 alpha, TNF-alpha) but not of other cytokines (IL-4). This imbalance in cytokine production in HTLV-I carriers may be related to the development of opportunistic infections and/or HTLV-I associated diseases including adult T-cell leukemia/lymphoma.

摘要

我们研究了I型人类嗜T淋巴细胞病毒(HTLV-I)携带者外周血单个核细胞(PBMC)在短期体外培养过程中干扰素γ(IFN-γ)、白细胞介素4(IL-4)、IL-1α和肿瘤坏死因子α(TNF-α)的产生情况,并与HTLV-I血清阴性对照者的PBMC进行了比较。从8名携带者和8名对照者中分离出PBMC进行培养,并在培养1天和3天的上清液中检测细胞因子水平。在所有HTLV-I携带者中均观察到IFN-γ产生增强,而对照者中均未出现。除一名有弓形虫淋巴结炎病史的携带者外,其他携带者的IL-4产生并未增加。携带者的IL-1α和TNF-α水平较高。CD4+细胞导致IFN-γ产生增强,而单核细胞导致IL-1α和TNF-α产生增加。本研究表明,HTLV-I携带者的PBMC持续产生大量某些细胞因子(IFN-γ、IL-1α、TNF-α),但不产生其他细胞因子(IL-4)。HTLV-I携带者细胞因子产生的这种失衡可能与机会性感染和/或包括成人T细胞白血病/淋巴瘤在内的HTLV-I相关疾病的发生有关。

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