ArticleThe Journal of experimental medicine1998
Interleukin 2-mediated uncoupling of T cell receptor alpha/beta from CD3 signaling.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- The pool of preactivated Lck in the initiation of T-cell signaling: a critical re-evaluation of the Lck standby model.Immunology and cell biology · 2015Article
- Lck, Membrane Microdomains, and TCR Triggering Machinery: Defining the New Rules of Engagement.Frontiers in immunology · 2012Article
- The adaptor protein SAP directly associates with CD3ζ chain and regulates T cell receptor signaling.PloS one · 2012Article
- Peripherally induced human regulatory T cells uncouple Kv1.3 activation from TCR-associated signaling.European journal of immunology · 2011Article
- Direct observation and quantitative analysis of Lck exchange between plasma membrane and cytosol in living T cells.The Journal of biological chemistry · 2010Article
- Lck-dependent Fyn activation requires C terminus-dependent targeting of kinase-active Lck to lipid rafts.The Journal of biological chemistry · 2008Article
- Regulation of Fyn through translocation of activated Lck into lipid rafts.The Journal of experimental medicine · 2003Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell activation and clonal expansion is the result of the coordinated functions of the receptors for antigen and interleukin (IL)-2. The protein tyrosine kinase p56(lck) is critical for the generation of signals emanating from the T cell antigen receptor (TCR) and has also been demonstrated to play a role in IL-2 receptor signaling. We demonstrate that an IL-2-dependent, antigen-specific CD4(+) T cell clone is not responsive to anti-TCR induced growth when propagated in IL-2, but remains responsive to both antigen and CD3epsilon-specific monoclonal antibody. Survival of this IL-2-dependent clone in the absence of IL-2 was supported by overexpression of exogenous Bcl-xL. Culture of this clonal variant in the absence of IL-2 rendered it susceptible to anti-TCR-induced signaling, and correlated with the presence of kinase-active Lck associated with the plasma membrane. The same phenotype is observed in primary, resting CD4(+) T cells. Furthermore, the presence of kinase active Lck associated with the plasma membrane correlates with the presence of ZAP 70-pp21zeta complexes in both primary T cells and T cell clones in circumstances of responsive anti-TCR signaling. The results presented demonstrate that IL-2 signal transduction results in the functional uncoupling of the TCR complex through altering the subcellular distribution of kinase-active Lck.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.