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人嗜T淋巴细胞病毒III型/淋巴腺病相关病毒感染时白细胞介素2的产生:抗原诱导的白细胞介素2产生缺陷但丝裂原诱导的白细胞介素2产生正常的证据

Interleukin 2 production in HTLV-III/LAV infection: evidence of defective antigen-induced, but normal mitogen-induced IL-2 production.

作者信息

Antonen J, Krohn K

出版信息

Clin Exp Immunol. 1986 Sep;65(3):489-96.

Abstract

We studied mitogen- and antigen-induced interleukin 2 (IL-2) production in HTLV-III/LAV infected and non-infected individuals and compared the results with T cell subpopulations, and with mitogen- and antigen-induced DNA synthesis and production of leucocyte migration inhibitory factor (LIF) in order to understand the controversial findings related to IL-2 production in HTLV-III/LAV infection. The HTLV-III/LAV antibody positive group showed immunological defects: low T helper (Th) cells, high T-suppressor (Ts) cells, reduced mitogen- and antigen-induced DNA-synthesis, but LIF production comparable to the HTLV-III/LAV antibody negative group. The total amount of IL-2, produced either as a response to a mitogenic stimulus or as a response to a soluble antigenic (purified protein derivative of tuberculin, PPD) stimulus, was lower in the HTLV-III/LAV antibody positive group. However, adjusting the IL-2 production to the amount of Th-cells showed that the IL-2 produced by a standard number of Th-cells after mitogen induction was similar in HTLV-III/LAV infected and non-infected individuals. In contrast, the ability of Th-cells of infected persons to produce IL-2, or to proliferate as a response to a soluble antigenic stimulus, was considerably diminished. We conclude that HTLV-III infection leads to a selective incapability to mount a specific Th-cell response either due to an intrinsic defect in the Th-cell population or due to metabolic and/or functional disturbances in antigen-processing and presenting accessory cells.

摘要

我们研究了丝裂原和抗原诱导的白细胞介素2(IL-2)在HTLV-III/LAV感染个体和未感染个体中的产生情况,并将结果与T细胞亚群、丝裂原和抗原诱导的DNA合成以及白细胞迁移抑制因子(LIF)的产生进行比较,以了解与HTLV-III/LAV感染中IL-2产生相关的有争议的发现。HTLV-III/LAV抗体阳性组表现出免疫缺陷:T辅助(Th)细胞数量低,T抑制(Ts)细胞数量高,丝裂原和抗原诱导的DNA合成减少,但LIF产生与HTLV-III/LAV抗体阴性组相当。无论是对丝裂原刺激还是对可溶性抗原(结核菌素纯化蛋白衍生物,PPD)刺激产生的IL-2总量,在HTLV-III/LAV抗体阳性组中都较低。然而,将IL-2产生量调整到Th细胞数量后发现,丝裂原诱导后标准数量的Th细胞产生的IL-2在HTLV-III/LAV感染个体和未感染个体中相似。相比之下,感染者的Th细胞产生IL-2或对可溶性抗原刺激进行增殖的能力明显减弱。我们得出结论,HTLV-III感染导致选择性地无法产生特异性Th细胞反应,这要么是由于Th细胞群体的内在缺陷,要么是由于抗原处理和呈递辅助细胞中的代谢和/或功能紊乱。

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