Research ArticleImmunology

T Cell Receptor–Dependent Activation of mTOR Signaling in T Cells Is Mediated by Carma1 and MALT1, But Not Bcl10

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Science Signaling  10 Jun 2014:
Vol. 7, Issue 329, pp. ra55
DOI: 10.1126/scisignal.2005169

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Delineating an Alternative Path to mTOR in T Cells

Antigen-dependent stimulation of the T cell receptor (TCR) leads to activation of the kinases PI3K, Akt, and mTOR, which are required for the proliferation of T cells and the increased metabolism that is needed to support their immune function. Hamilton et al. investigated the mechanism through which the TCR activates mTOR and identified a pathway independent of the best known upstream mTOR-activating kinase, Akt. Instead, proteins typically associated with a complex that transmits signals from the TCR to the transcription factor NF-κB were involved. Loss of either the adaptor protein Carma1 or the protease MALT1 in T cell lines blocked their proliferation in response to TCR stimulation. In addition, inhibition of MALT1 activity in primary human T cells inhibited their increased metabolism. Thus, Carma1 and MALT1 may form distinct signaling complexes to transmit signals from the TCR to different downstream effectors.