Breakthrough for Leicester toxicologists

Posted by mjs76 at Mar 12, 2010 12:30 PM |
Among the various facilities hosted by the University of Leicester is the world's longest-established toxicology research unit, where researchers have made a significant breakthrough in our understanding of human immune response.

Dr Melania Capasso and colleagues in the Medical Research Council Toxicology Unit, working with researchers from Cambridge, Oxford, Birmingham, Illinois and Vancouver, studied a recently discovered protein called HVCN1 which is a ‘voltage-gated proton channel’. In a nutshell, HVCN1 forms a passageway through the membrane of a cell, allowing the transfer of protons in and out, and is switched on and off by changes in the minuscule electrical current present in all living things. This movement of positively-charged protons affects oxidation reactions within the cell which in turn affect the activation of B cells, a type of lymphocyte.

If you understood that and want to know any more, feel free to read the paper which has been published in Nature Immunology. Or, if the immunological effects of sub-atomic particles isn’t your bag, just consider that HVCN1 is important in how the human body fights conditions such as cancer or rheumatoid arthritis, so the absence of HVCN1 is a bad thing. But knowing this is a good thing.

Other Leicester-based researchers on the project were Mandeep Bhamrah, Robert Boyd, Claudia Langlais, Kelvin Cain and David Dinsdale.

The MRC Toxicology Unit is one of the largest academic establishments in Europe devoted to toxicology and one of the longest-established medical research centres of any kind in the UK. Original conceived during the Second World War, it was set up at Porton Down in 1947 with a single member of staff.

Since 1991 it has been housed in a purpose built facility on the University of Leicester Campus and is home to nearly 100 researchers. The unit’s mission is to study and understand the fundamental mechanisms of toxicity, particularly mechanisms of cellular and tissue response to injury caused by drugs, chemicals and endogenous molecules.