CTLA-4-mediated inhibition in regulation of T cell responses: mechanisms and manipulation in tumor immunotherapy.
By C. Chambers, M. Kuhns, J. Egen, James P. Allison. Annual Review of Immunology, 2001
1,067 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/75b845f1093109e087cc28789de4cd83831485bb
How researchers see this paper
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In Immunology
- D. Pardoll
- J. Wolchok
- James P. Allison
- S. Rosenberg
- S. Topalian
- G. Freeman
- Alessandro Sette
- Bjoern Peters
In Oncology
- J. Wolchok
- D. Pardoll
- James P. Allison
- S. Rosenberg
- G. Freeman
- S. Topalian
- Charles G. Drake
- J. Massagué
Citations in the corpus
- Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4 (2013, background): “It is expressed on activated T cells and a subset of regulatory T cells (T reg cells; Chambers et al., 2001).”
- A clinical trial of CTLA-4 blockade with tremelimumab in patients with hepatocellular carcinoma and chronic hepatitis C. (2013, background): “The main role of CTLA-4 at the immune synapse is to outcompete the binding of the CD28 co-stimulatory receptor to CD80 and CD86 with much superior avidity [7,8].”
- CD28 and CTLA-4 coreceptor expression and signal transduction (2009, background): “In general, CTLA-4 is thought to raise the threshold for TCR signaling, thereby preventing responses to self-antigen (18, 136).”
- Novel immune checkpoint targets: moving beyond PD-1 and CTLA-4 (2019, background): “CTLA-4 is not detectable in naïve T cell but is rapidly induced upon T cell activation and it primarily regulates the amplitude of T cell during the early priming phase in lymphoid organs [29, 30].”