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在小鼠感染肥胖带绦虫的实验过程中,CD4 +和CD19 +脾细胞会发生凋亡。

CD4+ and CD19+ splenocytes undergo apoptosis during an experimental murine infection with Taenia crassiceps.

作者信息

López-Briones Sergio, Sciutto Edda, Ventura José Luis, Zentella Alejandro, Fragoso Gladis

机构信息

Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (UNAM), AP 70228, C.P. 04510, Mexico City, Mexico.

出版信息

Parasitol Res. 2003 Jun;90(2):157-63. doi: 10.1007/s00436-003-0829-2. Epub 2003 Feb 26.

Abstract

The Taenia crassiceps cysticercus is a cestode that naturally and experimentally infects rodents in which it reproduces by budding. In the laboratory, a persistent cellular immunosuppression with a concomitant increasing load of parasites has been observed in experimentally infected BALB/cAnN mice. In this study, enhanced apoptosis was found in spleen cells from 30-day infected mice with a typical "ladder-patterned" DNA fragmentation and an increase in phosphatidylserine expression. A characteristic poly-(ADP-ribose) polymerase cleavage indicates that this cell death is caspase-mediated. Apoptosis was detected in the CD4(+) and CD19(+) splenocytes of infected mice after in vitro stimulation with cysticercal antigens. Considering previous results on the crucial role that CD4(+) T cells play in controlling the extent of infection, apoptosis in this T-lymphocyte subpopulation induced by T. crassiceps cysticerci could be responsible for the immunosuppression that underlies parasite success.

摘要

肥胖带绦虫囊尾蚴是一种绦虫,可自然感染并通过实验感染啮齿动物,在啮齿动物体内通过出芽进行繁殖。在实验室中,在实验感染的BALB/cAnN小鼠中观察到持续的细胞免疫抑制,同时寄生虫负荷增加。在本研究中,在感染30天的小鼠脾脏细胞中发现凋亡增强,伴有典型的“梯状”DNA片段化和磷脂酰丝氨酸表达增加。特征性的多聚(ADP-核糖)聚合酶裂解表明这种细胞死亡是由半胱天冬酶介导的。在用囊尾蚴抗原体外刺激后,在感染小鼠的CD4(+)和CD19(+)脾细胞中检测到凋亡。考虑到先前关于CD4(+) T细胞在控制感染程度中起关键作用的结果,肥胖带绦虫囊尾蚴诱导的该T淋巴细胞亚群凋亡可能是寄生虫成功所依赖的免疫抑制的原因。

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