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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.

Original publication




Journal article



Publication Date





1691 - 1695


Adult, Alemtuzumab, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antibodies, Neoplasm, Antigens, CD, Antigens, Neoplasm, Antirheumatic Agents, B-Lymphocyte Subsets, CD4 Antigens, CD52 Antigen, Drug Administration Schedule, Female, Follow-Up Studies, Glycoproteins, Graves Disease, Humans, Lymphocyte Activation, Male, Methylprednisolone, Multiple Sclerosis, Chronic Progressive, Pulse Therapy, Drug, Receptors, Tumor Necrosis Factor, T-Lymphocyte Subsets, Th1 Cells, Thyroiditis, Autoimmune