BACKGROUND: Multiple sclerosis results from T-cell-dependent inflammatory 
demyelination of the central nervous system. Our objective was long-term 
suppression of inflammation with short-term monoclonal antibody treatment.
METHODS: We depleted 95% of circulating lymphocytes in 27 patients with multiple 
sclerosis by means of a 5-day pulse of the humanised anti-CD52 monoclonal 
antibody, Campath-1H. Clinical and haematological consequences of T-cell 
depletion, and in-vitro responses of patients' peripheral-blood mononuclear 
cells were analysed serially for 18 months after treatment.
FINDINGS: Radiological and clinical markers of disease activity were 
significantly decreased for at least 18 months after treatment. However, a third 
of patients developed antibodies against the thyrotropin receptor and 
carbimazole-responsive autoimmune hyperthyroidism. The depleted peripheral 
lymphocyte pool was reconstituted with cells that had decreased mitogen-induced 
proliferation and interferon gamma secretion in vitro.
INTERPRETATION: Campath-1H causes the immune response to change from the Th1 
phenotype, suppressing multiple sclerosis disease activity, but permitting the 
generation of antibody-mediated thyroid autoimmunity.