VLA-4 expression on peripheral blood lymphocytes is downregulated after treatment of multiple sclerosis with interferon beta
| Autor: | P. A. Calabresi, Henry F. Mcfarland, L. R. Tranquill, Clara M. Pelfrey, H. Maloni |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Adult
Integrins Multiple Sclerosis CD3 Complex medicine.medical_treatment Lymphocyte Receptors Lymphocyte Homing Integrin alpha4beta1 Biology Antibodies Flow cytometry Adjuvants Immunologic medicine Humans Lymphocytes Cell adhesion Receptor medicine.diagnostic_test Cell adhesion molecule Multiple sclerosis VLA-4 Interferon-beta Flow Cytometry medicine.disease Cytokine medicine.anatomical_structure Immunology Neurology (clinical) |
| Zdroj: | Neurology. 49:1111-1116 |
| ISSN: | 1526-632X 0028-3878 |
| Popis: | Adhesion molecules are likely to play a critical role in the immunopathogenesis of multiple sclerosis (MS). The interaction of vascular cell adhesion molecule-1 (VCAM-1) with its lymphocyte ligand very late antigen-4 (VLA-4) may mediate migration of lymphocytes into the CNS. We have previously demonstrated that MS patients treated with interferon beta(IFN-β) have a significant increase in soluble VCAM-1 (sVCAM-1) soon after the initiation of treatment, and this effect correlated with the resolution of contrast-enhancing MRI lesions. We studied the cell surface expression of VLA-4 by flow cytometry in 10 MS patients before and during IFN-β treatment. We found a significant decrease in mean VLA-4 fluorescence of MS patients' lymphocytes on treatment and no change in untreated controls. In vitro treatment of lymphocytes with IFN-β did not reproduce this effect, but the addition of sVCAM-1 did result in a decrease in VLA-4 expression. These data indicate that the previously identified increase in sVCAM-1 may lead to a decrease in VLA-4 expression and that this effect may partially explain the mechanism of action of IFN-β. |
| Databáze: | OpenAIRE |
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