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高密度和低密度PHA-(而非ConA-)激活的T细胞刺激自体混合淋巴细胞反应。

High and low density PHA- (but not ConA-) activated T cells stimulate the autologous mixed lymphocyte reaction.

作者信息

Brahmi Z, Thomas J E

出版信息

Ann Inst Pasteur Immunol (1985). 1985 Nov-Dec;136D(3):245-58. doi: 10.1016/s0769-2625(85)80110-0.

Abstract

In this study, PHA- and ConA-activated cells (PAC and CAC) were used as stimulators in mixed lymphocyte reactions (MLR) using autologous (auto) and allogeneic (allo) peripheral mononuclear cells as responders. PAC, but not CAC, were stimulatory in allo- and auto-MLR, and this stimulation was not due to residual PHA. In PAC which have been activated for 96 h, auto-MLR was due to determinants present on low density T-cell blasts, while with PAC which had been stimulated for more than 192 h, the determinants seemed to be associated with high density T cells. Anti-T3 monoclonal antibodies and certain anti-DR suppressed auto- and allo-MLR mediated by PAC when present throughout the entire MLR assays. CAC suppressed PAC-mediated auto-MLR in a dose-dependent fashion. This inhibition was not DR-restricted and was reversed by the addition of exogenous IL-2. Our results indicate that: depending upon the length of activation, both low density and high density PHA-activated T cells exhibited strong stimulatory capacity in auto-MLR; ConA-activated T cells failed to stimulate auto- or allo-MLR and suppressed MLR mediated by PAC; this suppression was due to suppressor cells, not to suppressor factors, and was readily reversed by exogenous IL-2; pretreatment of CAC with anti-TAC did not reverse the inhibition.

摘要

在本研究中,使用PHA和ConA激活的细胞(PAC和CAC)作为刺激物,在混合淋巴细胞反应(MLR)中,以自体(auto)和异体(allo)外周单个核细胞作为反应细胞。PAC而非CAC在异体和自体MLR中具有刺激作用,且这种刺激并非由于残留的PHA所致。在已激活96小时的PAC中,自体MLR归因于低密度T细胞母细胞上存在的决定簇,而对于已刺激超过192小时的PAC,这些决定簇似乎与高密度T细胞相关。当在整个MLR试验中全程存在时,抗T3单克隆抗体和某些抗DR抗体可抑制由PAC介导的自体和异体MLR。CAC以剂量依赖方式抑制PAC介导的自体MLR。这种抑制不受DR限制,并且可通过添加外源性IL-2而逆转。我们的结果表明:根据激活时间长短,低密度和高密度PHA激活的T细胞在自体MLR中均表现出强大的刺激能力;ConA激活的T细胞未能刺激自体或异体MLR,并抑制由PAC介导的MLR;这种抑制是由于抑制性细胞而非抑制因子所致,并且可被外源性IL-2轻易逆转;用抗TAC预处理CAC不能逆转这种抑制作用。

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