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[21] [22] In the early 1990s, James Allison showed that CTLA-4 acts as an inhibitory molecule to restrict T-cell responses. In 1996, Allison was the first to show that antibody blockade of a T-cell inhibitory molecule (known as CTLA-4 ) could lead to enhanced anti-tumor immune responses and tumor rejection.
CTLA-4 is a member of the immunoglobulin superfamily that is expressed by activated T cells and transmits an inhibitory signal to T cells. CTLA-4 is homologous to the T-cell co-stimulatory protein, CD28, and both molecules bind to CD80 and CD86, also called B7-1 and B7-2 respectively, on antigen-presenting cells. CTLA-4 binds CD80 and CD86 with ...
[14] [12] In the lab of James P. Allison at UC Berkeley, Krummel conducted key studies on the function of the protein CTLA-4; together they developed and described the first CTLA-4 inhibitors. They subsequently collaborated to apply the same inhibitors in tumor models, providing data on the blockade of inhibitory receptors can augment tumor ...
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They were able to demonstrate that CTLA-4 signaling in T cells inhibited T cell responses. [76] They then injected intact antibodies and demonstrated that CTLA-4 blockade enhanced T cell responses in mice responding to vaccines and to super antigens. [77] Leach, a new postdoctoral fellow, was tasked by Allison with applying these in tumor models.
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