Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis.
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 multi...
| Main Authors: | , , , , , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
1999
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| _version_ | 1797064557559021568 |
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| author | Coles, A Wing, M Smith, S Coraddu, F Greer, S Taylor, C Weetman, A Hale, G Chatterjee, V Waldmann, H Compston, A |
| author_facet | Coles, A Wing, M Smith, S Coraddu, F Greer, S Taylor, C Weetman, A Hale, G Chatterjee, V Waldmann, H Compston, A |
| author_sort | Coles, A |
| collection | OXFORD |
| description | 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. |
| first_indexed | 2024-03-06T21:16:04Z |
| format | Journal article |
| id | oxford-uuid:3fd3f5be-ec50-4581-ab8f-3bcd764b734b |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T21:16:04Z |
| publishDate | 1999 |
| record_format | dspace |
| spelling | oxford-uuid:3fd3f5be-ec50-4581-ab8f-3bcd764b734b2022-03-26T14:34:27ZPulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:3fd3f5be-ec50-4581-ab8f-3bcd764b734bEnglishSymplectic Elements at Oxford1999Coles, AWing, MSmith, SCoraddu, FGreer, STaylor, CWeetman, AHale, GChatterjee, VWaldmann, HCompston, A 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. |
| spellingShingle | Coles, A Wing, M Smith, S Coraddu, F Greer, S Taylor, C Weetman, A Hale, G Chatterjee, V Waldmann, H Compston, A Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title | Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title_full | Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title_fullStr | Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title_full_unstemmed | Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title_short | Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. |
| title_sort | pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis |
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