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Immunol Rev. 2010 Jul;236:54-67. doi: 10.1111/j.1600-065X.2010.00920.x.

Contracting the 'mus cells'--does down-sizing suit us for diving into the memory pool?

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  • 1Division of Immunobiology, Department of Pediatrics, University of Cincinnati, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.


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.

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