| 研究概要 |
T cell migration from circulation to the locus of inflammation may play an important role in the pathogenesis of autoimmune diseases, such as rheumatoid arthritis and Sjogren's syndrome. We have developed an in vitro model of blood vessels by culturing endothelial cells (EC) obtained from human umbilical cord veins as monolayr on collagen gels in tissue culture plate. Thus, after co-culturing T cells from peripheral blood on EC monolayr, T cells migrated through EC, as well as T cells that adhered to EC but did not migrate, were counted. Those T cells could also be recovered from collagen gels for the assessment of their surface phenotypes.
T cells that can migrate through endothelial cells, consist of a minor subset of CD4^+ helper T cells (1-5% of peripheral blood T cells) that strongly expressed activation-related antigens such as CD25, CD26, VLA-2 and VLA-3. Pretreatment of T cells with anti-VLA-3 antibody, or EC with anti-laminin antibody significantly inhibited the migration of T cells through EC monolayrs.
The number of migrating T cell subset in peripheral blood lymphocytes was decreased in patients with rheumatoid arthritis, as compared to normal subjects of patients with osteoarthritis. Patients with clinically more active synovitis had more decreased migrating T cells. Treatment with gold compound (GST) significantly decreased the number of migrating T cells probably by inhibiting the activation and production of migrating T cell subset.
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