- Meeting abstract
Plasma-cell like morphotype with loss of CD3 expression by Th1 cytokine producing cells
Arthritis Res Ther volume 5, Article number: 54 (2003)
Background and objective
Activated T helper CD4+ T cells, by their production and secretion of cytokines, seem to have functional similarities with plasmocytes secreting immunoglobulins. The morphotype and phenotype of IL-17- and IFN-γ-producing cells in both in vitro and in vivo situations remain to be clarified. Oligoclonal activation of normal peripheral blood mononuclear cells with the superantigen SEB and polyclonal activation with PMA/PHA for 4, 24, and 48 hours were used as in vitro models. This study was extended to various in vivo situations such as RA, dermatomyositis (DM), and normal activated lymph nodes.
We looked at the phenotype of IL-17 and IFN-γ-producing cells by immunohistochemistry, using the CD3 and CD4 T-cell markers, the CD20 B-cell marker, the CD38, and the kappa and lambda light-chain immunoglobulins plasmocytes markers. We also focused on the expression of two chemokine receptors, CCR6 and CCR7, involved with their associated ligands CCL20 and CC19/CCL21 in the migration of T lymphocytes.
Results and conclusions
IL-17 and IFN-γ-producing cells acquire a plasma-cell-like morphotype associated with the reduced expression of CD3 and the persistence of CD4 after both polyclonal and oligoclonal activation. In RA, DM, and activated lymph nodes, IL-17- and IFN-γ-producing cells presented the same morphotype. In RA synovium, these plasmacytoid-like Th1-producing cells still express the CD4 marker but not the CD3 and are CD20-, CD38-, kappa- and lambda-. In both in vitro and in vivo conditions, some of the Th1-producing cells can produce the CCR6 and CCR7 chemokine receptors, a finding which supports the argument that CCL20/CCR6 and CCL19,21/CCR7 play a role in the homing of T cells.
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Cite this article
Page, G., Sattler, A., Thiel, A. et al. Plasma-cell like morphotype with loss of CD3 expression by Th1 cytokine producing cells. Arthritis Res Ther 5 (Suppl 1), 54 (2003). https://doi.org/10.1186/ar684