Find out more about the Institute's research on CTLA-4.
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Our lab is interested in the fundamental mechanisms which regulate T cells within our immune system.
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Whilst most of the time T cells like to fight invaders such as bacteria and viruses, when things go wrong we can get a number of diseases including: Rheumatoid arthritis, Type-I diabetes, Multiple sclerosis, Inflammatory bowel diseases, Immune deficiencies, Transplant rejection.
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By destroying CD86, CTLA-4 can prevent CD28 from activating immune responses. This is carried out by specialised regulatory T cells.
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CD28 and CTLA-4 are the molecular checkpoint representing immunity to pathogens and immunity to self.
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CTLA-4 is highly dynamic and moves rapidly around inside the cell in vesicles, briefly visiting the cell surface.
![CD80 and CD86](https://www.ucl.ac.uk/immunity-transplantation/sites/immunity_transplantation/files/styles/large_image/public/427-sansom-ctla-6.jpg?itok=0BttEYue)
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Lymph nodes are bean-like structures that swell up every time you get a sore throat. Here T cells and antigen presenting cells (APC) meet. We are interested in what happens when these cells contact each other.
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CTLA-4 crystal structure showing position of deleterious amino acid mutations (red).