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来自HIV-1感染个体的树突状细胞刺激自体T细胞增殖的能力降低。

Dendritic cells from HIV-1 infected individuals show reduced capacity to stimulate autologous T-cell proliferation.

作者信息

Roberts M, Gompels M, Pinching A J, Knight S C

机构信息

Antigen Presentation Research Group, St Mary's Hospital Medical School, Northwick Park Institute for Medical Research, Harrow, UK.

出版信息

Immunol Lett. 1994 Dec;43(1-2):39-43. doi: 10.1016/0165-2478(94)00147-2.

Abstract

Dendritic cells (DC) exposed for a short period of time (1 day) in vitro to HIV infection caused stimulation of autologous T-cells, but those exposed for a longer period (3 days) before addition to T-cells stimulate little or no proliferation [1]. Since a proportion of DC from patients who are HIV-1 seropositive is infected with HIV-1 [2] we used the same culture system to test the level of ongoing stimulation of autologous T-cells by DC. The DC from patients with HIV-1 infection showed no enhanced stimulation of autologous T-cells; they produced significantly lower levels of proliferation than those induced by DC from normal controls or from high risk seronegative individuals. However, DC stimulated production of antibodies to gp120 and p24 in cultures containing autologous B plus T-cell in the absence of any added exogenous antigens as previously described [3]. DC in asymptomatic individuals thus appear to be fuelling antibody production but not T-cell proliferation. The results suggest that a failure by DC to stimulate T-cell proliferation either to HIV-1 or to other environmental antigens may be involved in the failure of cell-mediated responses in HIV infection.

摘要

在体外短时间(1天)暴露于HIV感染的树突状细胞(DC)可刺激自体T细胞,但在加入T细胞之前长时间(3天)暴露的DC几乎不刺激或不刺激T细胞增殖[1]。由于一部分HIV-1血清阳性患者的DC被HIV-1感染[2],我们使用相同的培养系统来测试DC对自体T细胞的持续刺激水平。来自HIV-1感染患者的DC未显示出对自体T细胞的增强刺激;它们产生的增殖水平明显低于正常对照或高危血清阴性个体的DC所诱导的增殖水平。然而,如先前所述[3],在没有任何添加的外源性抗原的情况下,DC在含有自体B细胞加T细胞的培养物中刺激产生针对gp120和p24的抗体。因此,无症状个体中的DC似乎在促进抗体产生而非T细胞增殖。结果表明,DC未能刺激针对HIV-1或其他环境抗原的T细胞增殖可能与HIV感染中细胞介导反应的失败有关。

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