Reversal of the TCR Stop Signal by CTLA-4

By H. Schneider, Jos Downey, Andrew Smith, Bernd H Zinselmeyer, C. Rush, J. Brewer, B. Wei, N. Hogg, P. Garside, C. Rudd. Science, 2006

645 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/2d29346a14b18f4c9d2332b610dc98119d5297fa

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. B. Fife
2. M. Krummel
3. D. Munn
4. J. Bluestone

In Immunology

1. P. Krammer
2. Angelika Schmidt
3. Nina Oberle
4. B. Fife
5. J. Wolchok
6. J. Bluestone
7. James P. Allison
8. Q. Tang

Citations in the corpus

• Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4 (2013, background): “CTLA-4 engagement by its ligands, B7-1 and B7-2, decreases IL-2 transcription, T cell proliferation, and T cell–APC contact times (Krummel and Allison, 1996; Schneider et al., 2006).”
• CTLA-4 and PD-1 Pathways (2016, background): “Proposed mechanisms for such inhibitory signals include direct inhibition at the TCR immune synapse, inhibition of CD28 or its signaling pathway, or increased mobility of T cells leading to decreased ability to interact with APCs.(9,12,13) CTLA-4 itself is subject to regulation, particularly by loca”
• CD28 and CTLA-4 coreceptor expression and signal transduction (2009, background): “It could also account for increased tissue infiltration by Ctla-4 ⁄ ) T cells, and the fact that the coreceptor is not expressed on naive and resting T cells which require longer dwell times with APCs for activation (26, 27).”
• Interactions between programmed death-1 and programmed death ligand-1 promote tolerance by blocking the T cell receptor-induced stop signal (2009, background): “Two reports have investigated the effect of CTLA-4 on T cell stop signal”
• Cytotoxic CD8+ T cells in cancer and cancer immunotherapy (2020, background): “CTLA-4 activation interferes with CD8 T-cell movements and the ability to form stable conjugates with APCs, thus reducing the contact time between cells.(33) While PD-1 signals are effective during the effector phase and predominantly occur within the peripheral tissues,(34) CTLA-4 signals are effec”
• The emerging role of CTLA4 as a cell-extrinsic regulator of T cell responses (2011, background): “Such a model predicts that the expression of CTLA4 keeps T cells mobile, preventing them from being inappropriately primed by APC”
• Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “Previous reports by Rudd and colleagues (103) have suggested that CTLA-4 engagement actually led to decreased movement and velocities of CD4(1) T cells, concluding that CTLA-4 normally enhances the stop signal and firm T-cell interactions with DCs.”
• Molecular Mechanisms of Treg-Mediated T Cell Suppression (2012, background): “), transduction of negative signals that induce cell cycle arrest and prevent IL-2 secretion (Krummel and Allison, 1996; Walunas et al., 1996), and limiting T cell contact with APCs (Schneider et al., 2006).”
• Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2 (2012, background): “The two major negative costimulatory receptors, CTLA-4 and PD-1, were reported to disrupt the TCRmediated stop signal, resulting in instability of synapse formation (Schneider et al., 2006; Fife et al., 2009).”