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- W2039236540 abstract "The adaptive immune system generates protective T cell responses via a poorly understood selection mechanism that favors expansion of clones with optimal affinity for antigen. Here we showed that upon T cell activation, the proapoptotic molecule Noxa (encoded by Pmaip1) and its antagonist Mcl-1 were induced. During an acute immune response against influenza or ovalbumin, Pmaip1(-/-) effector T cells displayed decreased antigen affinity and functionality. Molecular analysis of influenza-specific T cells revealed persistence of many subdominant clones in the Pmaip1(-/-) effector pool. When competing for low-affinity antigen, Pmaip1(-/-) TCR transgenic T cells had a survival advantage in vitro, resulting in increased numbers of effector cells in vivo. Mcl-1 protein stability was controlled by T cell receptor (TCR) affinity-dependent interleukin-2 signaling. These results establish a role for apoptosis early during T cell expansion, based on antigen-driven competition and survival of the fittest T cells." @default.
- W2039236540 created "2016-06-24" @default.
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- W2039236540 date "2010-06-01" @default.
- W2039236540 modified "2023-10-14" @default.
- W2039236540 title "Apoptosis Threshold Set by Noxa and Mcl-1 after T Cell Activation Regulates Competitive Selection of High-Affinity Clones" @default.
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- W2039236540 doi "https://doi.org/10.1016/j.immuni.2010.06.005" @default.
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