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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 ...
[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.
Bluestone's lab published studies, one together with Krummel and Allison, for in vitro studies of CTLA-4 function. [78] [79] In collaboration with Mark Jenkins, they were able to see effects of anti-CTLA-4 antibodies in vivo in an immunization setting, [80] but did not effectively carry this into tumor biology. Linsley and colleagues had made ...
These are most likely due to the breadth of the induced T-cell activation when anti-CTLA-4 antibodies are administered by injection in the blood stream. Using a mouse model of bladder cancer, researchers have found that a local injection of a low dose anti-CTLA-4 in the tumour area had the same tumour inhibiting capacity as when the antibody ...
1995 – James P. Allison is the first to describe the function of the critical immune checkpoint CTLA-4; 1995 – Regulatory T cells (Shimon Sakaguchi) 1995 – First Dendritic cell vaccine trial reported by Mukherji et al. 1995 – Discovery of the insect Imd NF-κB pathway [18]
The Breakthrough is written for the lay reader and includes sections on immunology that have been written for a general audience. It examines the development of cancer immunotherapy, starting with William Coley's work with toxins in the 1890s, moving on to the long hiatus of immunotherapy, and concluding with victory for the believers in the form of regulatory approval of CTLA-4, PD-1, and PD ...
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