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凋亡作为实验性恰加斯病中T细胞无反应性的一个原因。

Apoptosis as a cause of T-cell unresponsiveness in experimental Chagas' disease.

作者信息

Lopes M F, DosReis G A

机构信息

Departamento de Imunologia, Universidade Federal do Rio de Janeiro, Brasil.

出版信息

Braz J Med Biol Res. 1995 Aug;28(8):913-8.

PMID:8555995
Abstract

A murine model of Chagas' disease induced by metacyclic forms of T. cruzi was used to evaluate T-cell function during infection. T-cell unresponsiveness to TcR;CD3 stimulation in vitro and lymphocyte activation in vivo occurred simultaneously. These paradoxical findings are discussed in the light of recent evidence that mature activated T cells become susceptible to TcR-mediated apoptosis. Activation-induced death in T cells from T. cruzi-infected mice has recently been demonstrated in this model. Evidence that TcR-induced death of activated T cells could be a cause for T-cell unresponsiveness in vitro and in vivo, as well as the possible molecular mechanisms involved, are discussed.

摘要

使用由克氏锥虫的循环后期形式诱导的恰加斯病小鼠模型来评估感染期间的T细胞功能。体外T细胞对TcR;CD3刺激无反应和体内淋巴细胞活化同时发生。根据最近的证据,即成熟活化的T细胞易受TcR介导的细胞凋亡影响,对这些矛盾的发现进行了讨论。最近在该模型中已证明来自克氏锥虫感染小鼠的T细胞中的活化诱导死亡。讨论了TcR诱导的活化T细胞死亡可能是体外和体内T细胞无反应的原因以及所涉及的可能分子机制的证据。

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