Fas and perforin are not required for thymus atrophy induced by Trypanosoma cruzi infection
Fas and perforin are not required for thymus atrophy induced by Trypanosoma cruzi infection
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DOI：
10.1016/j.exppara.2004.04.010
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发表时间：
2004-05-01
影响因子：
2.1
通讯作者：
Araújo-Jorge, TC
中科院分区：
文献类型：
--
作者：
Henriques-Pons, A;DeMeis, J;Araújo-Jorge, TC
在克氏锥虫的急性期。感染后，胸腺明显萎缩，这是由大量未成熟的CD 4/CD 8双阳性细胞丢失决定的。最近，从寄生虫细胞膜脱落的寄生虫转醛酸酶的参与和嘌呤能受体P2 X（7）的激活被认为是导致胸腺萎缩的重要途径。在这项工作中，我们使用gldlgld和perform（-/-）小鼠评估了基于Fas和穿孔素的细胞毒性途径在克氏锥虫感染诱导的胸腺萎缩中的可能参与。我们发现在两种细胞毒性途径中有能力或缺乏的小鼠中胸腺萎缩的相似动力学，表明两种分子不直接参与胸腺萎缩，诱导细胞死亡或作为共刺激分子。(C)2004年爱思唯尔公司All rights reserved.
In the acute phase of Trypanosoma cruzi. infection there is a prominent thymus atrophy, which is determined by massive loss of immature CD4/CD8 double positive cells. Recently, the involvement of a parasite transialidase, which is shed from the parasite cell membrane and the activation of P2X(7), a purinergic receptor, were stated as important pathways leading to thymus atrophy. In this work we evaluated the possible involvement of Fas- and perforin-based cytotoxic pathways in the thymus atrophy induced by T cruzi infection using gldlgld and perform (-/-) mice, We found similar kinetics of thymus atrophy in mice competent or deficient in both cytotoxic pathways, indicating that both molecules are not directly involved in the thymus atrophy, either inducing cellular death or as co-stimulatory molecules. (C) 2004 Elsevier Inc. All rights reserved.