It has been almost three decades since the term "apoptosis" was first coined to describe a unique form of cell death that involves orderly, gene-dependent cell disintegration. It is now well accepted that apoptosis is an essential life process for metazoan animals and is critical for the formation and function of tissues and organs. In the adult mammalian body, apoptosis is especially important for proper functioning of the immune system. In recent years, along with the rapid advancement of molecular and cellular biology, great progress has been made in understanding the mechanisms leading to apoptosis. It is generally accepted that there are two major pathways of apoptotic cell death induction: extrinsic signaling through death receptors that leads to the formation of the death-inducing signaling complex (DISC), and intrinsic signaling mainly through mitochondria which leads to the formation of the apoptosome. Formation of the DISC or apoptosome, respectively, activates initiator and common effector caspases that execute the apoptosis process. In the immune system, both pathways operate; however, it is not known whether they are sufficient to maintain lymphocyte homeostasis. Recently, new apoptotic mechanisms including caspase-independent pathways and granzyme-initiated pathways have been shown to exist in lymphocytes. This review will summarize our understanding of the mechanisms that control the homeostasis of various lymphocyte populations.

译文

自从 “细胞凋亡” 一词首次被创造用来描述一种独特的细胞死亡形式以来,已经过去了近三十年,这种死亡形式涉及有序的基因依赖性细胞崩解。现在,人们普遍认为细胞凋亡是后生动物的基本生命过程,对于组织和器官的形成和功能至关重要。在成年哺乳动物体内,细胞凋亡对于免疫系统的正常运作尤其重要。近年来,随着分子生物学和细胞生物学的快速发展,人们对细胞凋亡机制的认识取得了很大进展。人们普遍认为,凋亡细胞死亡诱导有两种主要途径: 通过死亡受体的外在信号传导导致死亡诱导信号复合物 (DISC) 的形成,以及主要通过线粒体的内在信号传导导致细胞凋亡的形成。椎间盘或凋亡小体的形成分别激活执行凋亡过程的引发剂和常见的效应半胱天蛋白酶。在免疫系统中,两种途径都起作用; 但是,尚不清楚它们是否足以维持淋巴细胞的稳态。最近,淋巴细胞中存在新的凋亡机制,包括caspase非依赖性途径和颗粒酶启动途径。这篇综述将总结我们对控制各种淋巴细胞群体稳态机制的理解。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录