Modulation of cell-mediated immunity by lithium chloride.

Immunomodulation of cell-mediated immunity was studied in mice treated with either lithium chloride (LiCl), anti-CD8 monoclonal antibody or their combination. While 6-day LiCl treatment decreased the ability of their splenocytes to induce a local graft-versus-host reaction--anti-CD8 abolished this effect. The proliferative response of spleen cells from those three groups of mice to concanavalin A stimulation in vitro was significantly increased.

Protective effect of lithium on the stress-induced depression of cell-mediated immunity in mice.

The effect of lithium chloride (LiCl) administration on the stress-induced depression of cell-mediated immunity was studied in mice. Two models of stress-induced depression of immunity were used: (1) keeping the animals at a temperature of 4 degrees C twice for 24 h at a 24-h interval, and (2) keeping them in the dark for 96 h. Both kinds of stress significantly decreased the reactivity of cell donors in the graft-versus-host (GVH) reaction and recipients in the host-versus-graft (HVG) reaction.

Effect of immobilization stress on tumor growth in mice.

The effect of immobilization stress applied daily for 2 h on the development of MF-RSV tumor graft in mice and on survival of the hosts was studied. While a single acute stress applied to mice simultaneously with a transfer of MF-RSV cells stimulated antitumor defense, chronic stress applied both before and/or after tumor cell implantation accelerated the death of recipients. The shortest survival time was found in mice which were stressed for 3 weeks before implantation and on, until their death.

Stress-induced changes in muscarinic and beta-adrenergic binding sites on rat thymocytes and lymphocytes.

This study examined the effect of immobilization stress on the expression of muscarinic and beta-adrenergic receptors on thymocytes and lymphocytes obtained from 5-month-old L-E male rats. After 2 h immobilization (acute stress) there was a significant increase in specific binding of [3H]-DHA to beta-adrenergic receptors on thymocytes and on lymphocytes from the blood but not from the spleen, whereas [3H]-QNB binding to muscarinic receptors in those cells was not altered in comparison with the undisturbed control. Chronic immobilization stress (5 days, for 2 h) decreased the [3H]-QNB binding to lymphocytes collected from the spleen and blood but not from thymus; it caused neither a significant change in the 3H-DHA binding to thymocytes nor lymphocytes obtained from the blood and spleen.

Down-regulating effect on cellular immunity of the NSF17 factor produced by murine neonatal spleen cells fused with BW 5147 thymoma cells.

The non-specific factor NSF17 produced by mouse newborn splenocytes fused with BW 5147 thymoma cells was tested in vivo for its immunosuppressive activity. NSF17 administered i.p.

The influence of the age of donors and recipients on the regional graft-versus-host reaction in mice.

Regional graft versus host (GVH) reaction in mice induced by injection of parental strain spleen cells into the footpad of F1, recipients, was measured 7 days later by a popliteal lymph node (PLN) enlargement index. Young, 6-week-old F1 hosts can be used for studying the age- and sex-dependent GVH reactivity of parental strain donors. On the other hand, senescent, 21-24-month-old F1 recipients are able to mount a host versus graft response against parental antigens which may obscure the typical GVH reaction.

Effect of monosodium glutamate on cell-mediated immunity.

Cell-mediated immunity was investigated in adult mice and rats treated with monosodium glutamate in their suckling period. Delayed-type hypersensitivity to xenogeneic cells and host-versus-graft reactivity to allogeneic cells were depressed in these mice. Their splenocytes showed reduced mitogen-induced blastogenesis in vitro which was restored by removal of nonadherent to glass spleen cells.

The effect of lithium chloride treatment on cell-mediated immunity in mice.

The immunomodulatory effect of lithium chloride (LiCl) administered i.p. to adult mice (150 mg/kg/day) on cellular immunity in vivo was investigated.

Ontogenic development of immunoregulation in rats.

Suppressor activity of newborn rat spleen cells is totally inhibited on day 3 after birth by immunoregulatory cells of thymic origin. Contrasuppression represents a necessary, evolutionary step in the ontogenic development of the immune system.

Induction of indomethacin-sensitive suppressor cells by xenogeneic blood transfusion in mice.

The suppressive effect of xenogeneic blood transfusion on T-cell reactivity, observed in both in vivo and in vitro studies, is connected with the development of indomethacin-sensitive suppressor cells.

The role of prostaglandin E in the natural suppressor activity of spleen cells from newborn rats.

Spleen cells from newborn to 2-day-old, but not 3-day-old or older, rats suppress the activity of cells from adult animals in xenogeneic local graft-versus-host (GVH) assay. The duration of neonatal suppressor cell activity can be significantly prolonged by treating newborn rats with exogenous prostaglandin E2 (PGE2), and the suppression was completely abolished by administration of PGE inhibitor indomethacin. The results thus demonstrate an involvement of PGE2 in the mechanism of action of neonatal suppressor cells and may explain some discrepancies concerning the nature of natural suppressor cells present in newborn animals.

The disappearance of the foetal suppressor cell activity in newborn rats.

The suppressor splenocyte activity in newborn rats was studied using an intrarenal test of the local graft versus host reaction in the xenogenous rat-mouse system. It was demonstrated that the suppressor splenocyte activity in newborn rats born from both physiological and hormonally or mechanically prolonged pregnancy terminates within 2 days after birth. On the other hand, in newborn rats born from shortened pregnancy the suppressor splenocyte activity persists for 3 days.