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- W1574668619 abstract "The conventional paradigm of T cell activation through the TCR states that Lck plays a critical activating role in this signaling process. However, the T cell response to bacterial superantigens does not require Lck. In this study we report that not only is Lck dispensable for T cell activation by superantigens, but it actively inhibits this signaling pathway. Disruption of Lck function, either by repression of Lck gene expression or by selective pharmacologic inhibitors of Lck, led to increased IL-2 production in response to superantigen stimulation. This negative regulatory effect of Lck on superantigen-induced T cell responses required the kinase activity of Lck and correlated with early TCR signaling, but was independent of immunological synapse formation and TCR internalization. Our data demonstrate that the multistage role of Lck in T cell signaling includes the activation of a negative regulatory pathway of T cell activation." @default.
- W1574668619 created "2016-06-24" @default.
- W1574668619 creator A5009746498 @default.
- W1574668619 creator A5056785682 @default.
- W1574668619 date "2004-01-01" @default.
- W1574668619 modified "2023-10-03" @default.
- W1574668619 title "Superantigen Stimulation Reveals the Contribution of Lck to Negative Regulation of T Cell Activation" @default.
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- W1574668619 doi "https://doi.org/10.4049/jimmunol.172.1.222" @default.
- W1574668619 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14688329" @default.
- W1574668619 hasPublicationYear "2004" @default.
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