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Biomedical subjects

T Sakane

Publications and source records attributed to T Sakane.

At least 199 records · Page 11Linked to original sources
PubMed1982

Auto-oxidative damage in Behçet's disease--endothelial cell damage following the elevated oxygen radicals generated by stimulated neutrophils.

The functions of phagocytes are enhanced in patients with Behçet's disease, therefore, we investigated the neutrophil-derived oxygen intermediates (OI) and lysosomal enzymes from 17 patients receiving glucocorticosteroids (steroids) and colchicine. Cultured endothelial cells were incubated with neutrophils to assess tissue injury. In cases of the complete type, in the active stage of the disease, OI production was markedly increased. The other patients showed significantly higher OI and higher lysosomal enzyme levels than patients with other diseases (controls) receiving drug therapy. Cytotoxicity tests showed that the 51Cr release was also significantly higher. The destruction of desmosomes and cell deformation were demonstrated electron microscopically. The simultaneous addition of superoxide dismutase and catalase in the cell culture decreased the 51Cr release to control levels. These findings suggest that neutrophils from patients with Behçet's disease generate high levels of OI, resulting in endothelial tissue damage.

Adolescent↗
PubMed1981

Separation of concanavalin A-induced human suppressor and helper T cells by the autologous erythrocyte rosette technique.

Very few normal human peripheral blood T cells are capable of binding autologous erythrocytes to form rosettes, whereas in the T cell population activated by concanavalin A (Con A) the autorosette levels are markedly enhanced. Fractionation of the Con A-activated T cells with autologous erythrocytes into autorosetting and nonrosetting cells demonstrates that suppressor, but not helper, activity resides in the autorosetting population, whereas the reverse is true of the nonrosetting population. Both these activities are found to be Con A dependent. The Con A-induced human suppressor cells can be identified and separated from the Con A-induced human helper cells by the autorosette technique. Studies on the surface properties of autorosetting and nonrosetting T cells indicate that there is little correlation between the activated suppressor and helper T cell subsets defined by autorosette technique and either those defined by monoclonal antibodies (which are able to distinguish these subsets in the resting but not activated T cells) or those defined by Fc receptors. Since the autorosetting T cell population (which acts as suppressor cells) bears receptors for peanut agglutinin, the nature of Con A-induced human suppressor cells appears to be analogous to that of Con A-induced murine suppressor cells.

Antigens, Surface↗
PubMed1979

Studies of immune functions of patients with systemic lupus erythematosus.

In normal individuals T cells are stimulated to proliferate by autologous non-T cells; this is called the autologous mixed lymphocyte reaction (MLR). Previous studies demonstrated that such an autologous MLR was markedly impaired in patients with active systemic lupus erythematosus (SLE). To determine whether the defect resided in the responding cell or the stimulating cell, mixing experiments were performed using cells from identical twins. We identified two sets of identical twins discordant for SLE activity and correspondingly discordant in their degree of responsiveness in the autologous MLR. Reciprocal mixing experiments were performed in which T cells from one twin of each pair were mixed with non-T cells from the other twin of that pair. These studies indicated that patients with active SLE have a defect in the ability of non-T cells to stimulate as well as a defect in the ability of both Tgamma and Tnongamma cells to respond in the autologous MLR. Patients with inactive SLE have a defect only in responsiveness of Tgamma cells.

Adult↗
PubMed1979

Studies of immune functions of patients with systemic lupus erythematosus. Complement-dependent immunoglobulin M anti-thymus-derived cell antibodies preferentially inactivate suppressor cells.

Patients with systemic lupus erythematosus (SLE) produce excessive amounts of autoantibodies. It has also been demonstrated in several systems that such patients have a relative loss of suppressor thymus-derived (T) cells that inhibit the immune response. This loss of suppressor cells has been suggested as one of the causes of the excessive production of antibodies in patients with SLE. In the present report we have tested the hypothesis that anti-T-cell antibodies found in the plasma of some patients with SLE preferentially kill suppressor cells. T cells from normal individuals can be activated by concanavalin A to develop suppressor cell activity. We therefore cultured normal T cells together with concanavalin A in the presence of plasma or plasma fractions from patients with SLE. We found that plasma from patients with active SLE, in which anti-T-cell antibodies were present, inhibited the development of suppressor activity in such cultures. In contrast, plasma from other active patients and patients with inactive SLE, in which no anti-T-cell antibodies could be detected, failed to block the development of such suppressor activity. Absorption of the plasma that contained anti-T-cell antibodies with T cell, but not non-T cells, could eliminate the suppressor-inhibiting activity of the SLE plasma that contained anti-T-cell antibodies. The immunoglobulin (Ig)M, but not the IgG, fraction of the plasma was shown to possess the inhibiting property and complement was found to be necessary for the effect of such anti-T-cell antibodies. We also demonstrated that exposure of normal T cells to such anti-T-cell antibodies and complement did not affect another population of T cells that could proliferate in response to mitogens.Thus, certain patients with SLE have in their plasma an antibody of the IgM class that can selectively eliminate a population of T cells capable of developing suppressor function. The loss of suppressor T cells in patients with SLE may be the result of the effects of such antibody activity in vivo.

Adult↗
PubMed1979

Studies of immune functions of patients with systemic lupus erythematosus. T-cell subsets and antibodies to T-cell subsets.

Antibodies to T cells present in the plasma of patients with active systemic lupus erythematosus (SLE) plus complement are able to eliminate concanavalin A-induced suppressor function for the proliferative responses of T cells to allogeneic lymphocytes (MLR) and of B cells to pokeweed mitogen (PWM). Such antibodies were found to be effective in eliminating suppressor function only when T cells were treated before activation; there was no effect when treatment was performed after activation. These studies indicate that the antibodies preferentially interact with a T cell necessary for the generation of suppressor cells, rather than with mature, activated suppressor cells. Studies of individual SLE patients indicate that the same defects observed in SLE T cells were induced in normal T cells by plasma from that patient. Such observations suggest that many T-cell defects associated with active SLE may not be intrinsic T-cell abnormalities, but, rather, secondary effects of anti-T-cell antibodies. Studies of the T-cell subpopulations responsible for suppression of the MLR and PWM responses indicate that only T gamma cells (T cells bearing receptors for the Fc portion of immunoglobulin [Ig]G) acted as precursors of suppressor cells for the MLR, whereas both T gamma and T non-gamma cells (T cells not bearing receptors for the Fc portion of IgG) could be activated to suppress the PWM response. Consistent with this observation, SLE anti-T-cell antibodies that preferentially killed T gamma cells preferentially eliminated suppressor cells for the MLR.

Autoantibodies↗
PubMed1978

Failure of autologous mixed lymphocyte reactions between T and non-T cells in patients with systemic lupus erythematosus.

Normal human T cells proliferate vigorously when stimulated with autologous non-T cells. This autologous mixed lymphocyte reaction (MLR) between T and non-T cells was defective in patients with active systemic lupus erythematosus (SLE). In contrast, T cells and non-T cells from active SLE patients behaved normally as responding and stimulating cells, respectively, in the allogeneic MLR. The etiology of the impaired autologous MLR was further examined by studying the functional capacity of subsets of stimulating or responding cells. B cells, L cells, and monocytes from active SLE patients failed to stimulate autologous T cells but these cells effectively stimulated allogeneic T cells. Fc(IgG)+ T cells from active patients were unable to respond in both the autologous and allogeneic MLR; their Fc(IgG)-T cells responded well in the allogeneic but not in the autologous MLR. The Fc(IgG)+ T cells, but not the Fc(IgG)- T cells, from inactive SLE patients also failed to respond in the both autologous and allogeneic MLR. These studies indicate that patients with SLE have functionally defective Fc(IgG)+ T cells and a defective autologous MLR, both of which may contribute to impaired regulation of immune functions.

Adult↗