Therapeutic effects of monoclonal antibodies to alpha beta TCR but not to CD4 on collagen-induced arthritis in the rat
Autor: | T J Goldschmidt, Rikard Holmdahl |
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Rok vydání: | 1994 |
Předmět: |
musculoskeletal diseases
CD4-Positive T-Lymphocytes Male medicine.drug_class medicine.medical_treatment Receptors Antigen T-Cell alpha-beta T-Lymphocytes Immunology Arthritis Monoclonal antibody Lymphocyte Depletion medicine Animals Lymph node biology business.industry T-cell receptor Antibodies Monoclonal Immunotherapy T lymphocyte medicine.disease Rats medicine.anatomical_structure Immunization CD4 Antigens biology.protein Collagen Lymph Nodes Antibody business |
Zdroj: | Cellular immunology. 154(1) |
ISSN: | 0008-8749 |
Popis: | The role which T cells play in the pathogenesis of the collagen-induced arthritis (CIA) model is not yet fully understood. Although CIA is most likely dependent on the activity of class II-restricted CD4+ T cells, only prophylactic but not therapeutic anti-CD4 treatments have been successful. The lack of therapeutically effective anti-T cell monoclonal antibody treatments has questioned the importance of T cells in ongoing CIA. However, recently we found that ongoing CIA in DA rats induced with homologous CII can be suppressed by injections with an anti-alpha beta TCR antibody. Having a CIA model where ongoing disease was clearly dependent on T cells, we addressed in the present work whether also an anti-CD4 treatment could suppress ongoing arthritis in this model. Although no CD4hi lymph node cells were seen after an anti-CD4 injection, the arthritis was suppressed only after treatment at immunization but not after treatment just before onset of disease. In comparison, the anti-TCR treatment at the time of onset was clearly suppressive even though a large fraction of the T cells was not depleted. This indicates that the different outcome of the anti-TCR and anti-CD4 treatment was not due to a different capacity to deplete T cells in vivo. |
Databáze: | OpenAIRE |
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