Browsing by Author "Lukic, M.L. (7005792112)"

Spleen cells taken 4 days after lethal irradiation of Lewis rat were used as a source of radioresistant accessory cells. The transfer of 2x106 cells into syngeneic recipients significantly enhanced the antibody response to an immunogenic dose of SRBC, if given immediately prior to antigen. The enhancing effect was not observed if radioresistant cells were transferred 24 h or later after immunization. Elimination of adherent of phagocytic cells abolished the enhancing capacity of the radioresistant spleen cells. One hour pre-incubation in medium containing 0.4 mg/ml kappa carrageenan potentiated rather than inhibited the enhancing effect of radioresistant spleen cells. IgG PFC response appear to be more sensitive to the effect of the transferred spleen cells as compared with the direct (IgM) PFC response. It is concluded that activated splenic macrophages may enhance antibody response when transferred, at the time of immunization, into an immunocompetent host. Possible mechanisms of action are discussed.

Spleen cells taken 4 days after lethal irradiation of Lewis rat were used as a source of radioresistant accessory cells. The transfer of 2x106 cells into syngeneic recipients significantly enhanced the antibody response to an immunogenic dose of SRBC, if given immediately prior to antigen. The enhancing effect was not observed if radioresistant cells were transferred 24 h or later after immunization. Elimination of adherent of phagocytic cells abolished the enhancing capacity of the radioresistant spleen cells. One hour pre-incubation in medium containing 0.4 mg/ml kappa carrageenan potentiated rather than inhibited the enhancing effect of radioresistant spleen cells. IgG PFC response appear to be more sensitive to the effect of the transferred spleen cells as compared with the direct (IgM) PFC response. It is concluded that activated splenic macrophages may enhance antibody response when transferred, at the time of immunization, into an immunocompetent host. Possible mechanisms of action are discussed.

[No abstract available]

Pretreatment of epidermal cells (EC) with hydrocortisone or dexamethasone abolishes their capacity to produce interleukin-1 (IL-1) and therefore reduces their capacity to support proliferative response of lectin-stimulated T cells. Additionally, glucocorticoid-pretreated keratinocytes produce an inhibitor of IL-1 activity. This factor is a non-dialysable product of radioresistant epidermal cells, does not represent a non-specific inhibitor of DNA synthesis and appears to be specific for IL-1 since it did not interfere with IL-2-dependent T-cell proliferation. It affects both IL-2 production and the induction of IL-2-receptor expression. Finally, it blocks binding of IL-1 to its receptors on D10S subclone as evaluated by competitive binding assay. Thus, we have provided evidence which indicates that immunosuppressive effects of glucocorticoids in the skin may also be mediated by an IL-1 receptor antagonist(s) produced by keratinocytes.

Pretreatment of epidermal cells (EC) with hydrocortisone or dexamethasone abolishes their capacity to produce interleukin-1 (IL-1) and therefore reduces their capacity to support proliferative response of lectin-stimulated T cells. Additionally, glucocorticoid-pretreated keratinocytes produce an inhibitor of IL-1 activity. This factor is a non-dialysable product of radioresistant epidermal cells, does not represent a non-specific inhibitor of DNA synthesis and appears to be specific for IL-1 since it did not interfere with IL-2-dependent T-cell proliferation. It affects both IL-2 production and the induction of IL-2-receptor expression. Finally, it blocks binding of IL-1 to its receptors on D10S subclone as evaluated by competitive binding assay. Thus, we have provided evidence which indicates that immunosuppressive effects of glucocorticoids in the skin may also be mediated by an IL-1 receptor antagonist(s) produced by keratinocytes.

[No abstract available]

[No abstract available]

Herpes simplex virus (HSV) infection of mice can induce viral encephalitis. Using two-fluorochrome immunofluorescence, our present study shows that though there is extensive myelin loss and necrosis in the brain stem of mice with HSV encephalitis, only some oligodendrocytes, astrocytes and microglial cells are infected. T cells that express CD4 or CD8 and a large number of CD4+, F4/80+ macrophages are present in perivascular infiltrates close to and in contact with HSV-infected cells in areas of massive myelin loss. These findings suggest that the resultant infiltration of immune cells into the brain during HSV-1 infection may cause as much damage as the virus itself. © 1989.

Herpes simplex virus (HSV) infection of mice can induce viral encephalitis. Using two-fluorochrome immunofluorescence, our present study shows that though there is extensive myelin loss and necrosis in the brain stem of mice with HSV encephalitis, only some oligodendrocytes, astrocytes and microglial cells are infected. T cells that express CD4 or CD8 and a large number of CD4+, F4/80+ macrophages are present in perivascular infiltrates close to and in contact with HSV-infected cells in areas of massive myelin loss. These findings suggest that the resultant infiltration of immune cells into the brain during HSV-1 infection may cause as much damage as the virus itself. © 1989.

To investigate the role of IL-1 in nitric oxide (NO)-mediated destructive processes in the multiple low dose streptozotocin (MLD-STZ) induced model of autoimmune diabetes, CBA/H mice received 10 consecutive i.p. injections of either rat IL-1 inhibitor (IL-1 INH), or human recombinant IL-1 receptor antagonist (IL-1ra). In contrast to the control MLD-STZ group (40-45 mg/kg for 5 days) which developed persistent hyperglycemia associated with insulitis and islet cell destruction, both IL-1 INH- and rIL-1ra-treated mice were protected from the induction of the disease. Preliminary immunohistochemical studies indicated that the high local concentration of NO-producing enzyme NO synthase, present in control MLD-STZ islets, is significantly reduced in both experimental groups of mice where IL-1 activity was blocked either by IL-1 INH or rIL-1ra.

Water soluble fraction (SF) of SRBC was obtained by hypotonic lysis and ultracentrifugation. SF was found to induce very weak SRBC-specific antibody response in mice. Pretreatment with SF accelerated direct PFC response to SRBC and accelerated and suppressed indirect PFC response. Spleen cells from mice treated with SF exhibited enhanced response to SRBC after transfer in irradiated recipients. The transfer of spleen cells from mice treated with SF to normal non-irradiated mice markedly suppressed the recipients' PFC responses to SRBC. The observed suppressive effect is interpreted as a consequence of suppressor cell activity.

Water soluble fraction (SF) of SRBC was obtained by hypotonic lysis and ultracentrifugation. SF was found to induce very weak SRBC-specific antibody response in mice. Pretreatment with SF accelerated direct PFC response to SRBC and accelerated and suppressed indirect PFC response. Spleen cells from mice treated with SF exhibited enhanced response to SRBC after transfer in irradiated recipients. The transfer of spleen cells from mice treated with SF to normal non-irradiated mice markedly suppressed the recipients' PFC responses to SRBC. The observed suppressive effect is interpreted as a consequence of suppressor cell activity.

Susceptibility to the induction of EAE was compared in AO, DA and Lewis strain of rats. As evaluated by clinical and histological criteria, AO rats exhibited significantly lower susceptibility to EAE induced with guinea-pig spinal cord (GPSC) tissue and complete resistance to the encephalitogenic challenge with rat myelin basic protein (BP) irrespective of antigen dose and adjuvant used. AO rats pre-treated with BP + Freund's incomplete adjuvant became completely unresponsive to the induction of EAE with GPSC + Freund's complete adjuvant (FCA) indicating that they do possess cells sensitive to some antigenic determinants of rat BP. In order to test whether the resistance to EAE is due to an active suppression, low dose of irradiation (300 rad) and cyclophosphamide (20 mg/kg) was applied prior to the induction of EAE. Selective depletion of radiosensitive cells facilitated the induction of EAE. Similarly, cyclosphosphamide given 2 days prior to BP + FCA completly abrogated the resistance to EAE induction. Thus, it appears that the inability of BP + FCA to produce EAE in AO rats is due to the disproportionate activation of suppressor cells.