Spontaneous proliferation of and cytokine production by T cells adherent to human endothelial cells in patients with human T-lymphotropic virus type I-associated myelopathy.

We previously reported increased adherence of T cells to human endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM). To define the immunological function of EC-adherent T cells from HAM patients, we investigated the degree of spontaneous proliferation and the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and granulocyte-macrophage colony stimulating factor (GM-CSF). Both the degree of spontaneous proliferation and the production of TNF-alpha, IFN-gamma, and GM-CSF by EC-adherent T cells of HAM patients were significantly increased, compared to anti-HTLV-I seronegative controls. Furthermore, in HAM patients, spontaneous proliferation and production of inflammatory cytokines by EC-adherent T cells were significantly higher than that of EC-non-adherent T cells. Conversely, those functions of EC-non-adherent T cells were significantly lower than that of unseparated cells, which were T cells before application to EC. We demonstrated that EC-adherent T cells were qualitatively and quantitatively more hyperactive than those of anti-HTLV-I seronegative controls and the population of activated T cells of HAM patients was concentrated in EC-adherent T cells rather than in EC-non-adherent T cells. Our results suggest that EC-adherent T cells in the peripheral blood of HAM are intimately involved in the immunopathogenesis of HAM.