Contracting the 'mus cells'--does down-sizing suit us for diving into the memory pool?
Contracting the 'mus cells'--does down-sizing suit us for diving into the memory pool?
复制标题
DOI:
10.1111/j.1600-065x.2010.00920.x
复制
发表时间:
2010-07
影响因子:
8.7
通讯作者:
Hildeman DA
中科院分区:
文献类型:
--
作者:
Kurtulus S;Tripathi P;Opferman JT;Hildeman DA
Maintenance of T-cell homeostasis is critical for normal functioning of the immune system. After thymocyte selection, T cells enter the peripheral lymphoid organs, where they are maintained as naive cells. Transient disruption of homeostasis occurs when naive T cells undergo antigen-driven expansion and acquire effector functions. Effector T cells then either undergo apoptosis (i.e. contraction at the population level) or survive to become memory cells. This apoptotic process is crucial: it resets T-cell homeostasis, promotes protective immunity, and limits autoimmunity. Although initial studies using in vitro models supported a role for death receptor signaling, more recent in vivo studies have implicated Bcl-2 family members as being critical for the culling of T-cell responses. While several Bcl-2 family members likely contribute to T-cell contraction, the pro-apoptotic molecule Bim and its anti-apoptotic antagonist Bcl-2 are essential regulators of the process. This review discusses the progress made in our understanding of the mechanisms underlying contraction of T-cell responses and how some cells avoid this cell death and become memory T cells.