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Find out about Dr Coles' conclusions in the next part of his article
Dr Coles took part in a web chat and moderated discussion board answering questions from the public.
The story of Campath
The story of Campath-1H in multiple sclerosis
By Dr. Alasdair Coles, Department of Neurology
Addenbrooke's Hospital, Cambridge, UK
May 2nd 2007
The history of Campath-1H
In Cambridge, UK, in the 1970s a great breakthrough was made. Kohler and Milstein discovered a way of making antibodies, for which they would later receive the Nobel Prize. Their technique was special in two ways. First, they used a cell system which meant that the antibodies could be made perpetually. Secondly, the antibodies could be made 'monoclonal' so that the immortalised cells produce antibodies that all target the same molecule. This specificity led to their nickname, "magic bullets". Many drugs have been made using this technique, including Antegren (natalizumab) for multiple sclerosis.
Just opposite Kohler and Milstein's laboratory was Addenbrooke's Hospital and it was here that the prototype therapeutic monoclonal antibodies were first put to clinical use. One of these was (External)
Campath-1H
, an antibody that was extraordinarily effective at killing lymphocytes, which are a subset of the white cells in the blood that makes up the immune system
Initially it was used in conditions where lymphocytes are overproduced, such as leukaemias and lymphomas. It is now (External)
a licensed treatment for B cell chronic lymphocytic leukaemia
Campath-1H in progressive multiple sclerosis: 1991-8
By the early 1990s, doctors in Cambridge began to experiment with using Campath-1H in autoimmune diseases, such as rheumatoid arthritis and vasculitis. So it was that, in 1991, the first person with multiple sclerosis was treated using Campath-1H. She, and the next 35 patients, had secondary progressive multiple sclerosis. At one level, Campath-1H was very effective: it dramatically reduced relapse rate and new MRI lesion formation.(1,2,3). However, it had very little effect on the progression of their disability. We concluded, as many other people were doing at the time for other reasons, that the progressive phase of multiple sclerosis is not due to inflammation and therefore not amenable to anti-inflammatory treatments. Instead the progressive phase of multiple sclerosis is probably due to the slow death of nerve cells themselves.
The critical issue for the treatment of multiple sclerosis is whether this death of nerve cells can be prevented. At present, all we have available to us are drugs that act on the immune system to suppress inflammation and demyelination. Now, we believe that nerve cells die off in multiple sclerosis because they have lost the beneficial effects of their myelin wrapping. In which case, if we can suppress inflammation early enough, and prevent too much demyelination, we should be able to stop nerve cell death. This is a hypothesis only. Some neurologists think multiple sclerosis is primarily a disease where nerve cells are destined to die, and that the inflammation we see in the brain is secondary; in which case no anti-inflammatory treatment will prevent the progressive phase of multiple sclerosis.
Read about
Dr Coles conclusions
References
1:
Moreau T, Thorpe J, Miller D, Moseley I, Hale G, Waldmann H, Clayton D, Wing M, Scolding N, Compston A. Preliminary evidence from magnetic resonance imaging for reduction in disease activity after lymphocyte depletion in multiple sclerosis. Lancet. 1994 Jul 30;344(8918):298-301.
2:
Paolillo A, Coles AJ, Molyneux PD, Gawne-Cain M, MacManus D, Barker GJ,Compston DA, Miller DH. Quantitative MRI in patients with secondary progressive MS treated with monoclonal antibody Campath 1H.Neurology. 1999 Sep 11;53(4):751-7.
3:
Coles AJ, Wing MG, Molyneux P, Paolillo A, Davie CM, Hale G, Miller D,Waldmann H, Compston A. Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis.
Ann Neurol. 1999 Sep;46(3):296-304.
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