The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform
Hymie Anisman - One of the best experts on this subject based on the ideXlab platform.
-
stressor induced alterations of the splenic Plaque Forming Cell response strain differences and modification by propranolol
Pharmacology Biochemistry and Behavior, 1996Co-Authors: Leslie Kerr, Leslie Drummond, Marilee D Zaharia, Joanne Clelford, Hymie AnismanAbstract:Abstract The effects of stressor application on the splenic Plaque-Forming Cell (PFC) response was assessed in two strains of mice: the BALB/cByJ strain, which is highly responsive to stressors; and the more hardy DBA/2J strain. Both strains exhibited a peak PFC response 120 h following administration of sheep red blood Cells (SRBC; 5 × 106 Cells). Stressor exposure reduced the immune response; however, the appearance of such an outcome was dependent upon the time at which the stressor was applied relative to SRBC inoculation. In DBA/2J mice, foot-shock applied either immediately after SRBC inoculation or at the time of the peak immune response (120 h) resulted in suppression of the PFC response. In BALB/cByJ mice, both stressor severities provoked an immunosuppression when applied 120 h after inoculation, but when applied 96 h after immunization only foot-shock reduced the PFC response. At other intervals, the stressors were without effect. Pretreatment with the β-norepinephrine antagonist propranolol precluded the immunosuppression elicited by a stressor applied 96 h after inoculation, but did not affect the reduction of the PFC response elicited by a stressor applied 120 h after inoculation. It is suggested that several factors may contribute to stressor-provoked alterations of the immune response, and that the contribution of these factors vary over the course of an immune response being mounted.
F Sendo - One of the best experts on this subject based on the ideXlab platform.
-
modulation of the in vivo immune response by selective depletion of neutrophils using a monoclonal antibody rp 3 iii enhancement by rp 3 treatment of the anti sheep red blood Cell Plaque Forming Cell response in rats
Journal of Immunology, 1994Co-Authors: M Tamura, S Sekiya, M Terashita, F SendoAbstract:Because recent work has shown that neutrophils produce various cytokines and are activated by these agents, this study was undertaken to examine neutrophil participation in immune networks. In our previous work, we demonstrated that delayed type hypersensitivity to SRBC and accompanying mononuclear leukocyte recruitment are inhibited in vivo by selective depletion of neutrophils using a mAb designated RP-3. To elucidate the function of these Cells in Ab production, we assessed the splenic Plaque-Forming Cell response to SRBC in a rat model through selective depletion of circulating neutrophils by RP-3. This depletion which occurred at the time of immunization resulted in an increase in the number of anti-SRBC Ab producing Cells, as determined by the direct and indirect Plaque-Forming Cell response. This phenomenon was observed only when the Ag was administered i.p. and not with i.v. immunization. These results suggest that neutrophils suppress Ab production in certain situations.
Leslie Kerr - One of the best experts on this subject based on the ideXlab platform.
-
stressor induced alterations of the splenic Plaque Forming Cell response strain differences and modification by propranolol
Pharmacology Biochemistry and Behavior, 1996Co-Authors: Leslie Kerr, Leslie Drummond, Marilee D Zaharia, Joanne Clelford, Hymie AnismanAbstract:Abstract The effects of stressor application on the splenic Plaque-Forming Cell (PFC) response was assessed in two strains of mice: the BALB/cByJ strain, which is highly responsive to stressors; and the more hardy DBA/2J strain. Both strains exhibited a peak PFC response 120 h following administration of sheep red blood Cells (SRBC; 5 × 106 Cells). Stressor exposure reduced the immune response; however, the appearance of such an outcome was dependent upon the time at which the stressor was applied relative to SRBC inoculation. In DBA/2J mice, foot-shock applied either immediately after SRBC inoculation or at the time of the peak immune response (120 h) resulted in suppression of the PFC response. In BALB/cByJ mice, both stressor severities provoked an immunosuppression when applied 120 h after inoculation, but when applied 96 h after immunization only foot-shock reduced the PFC response. At other intervals, the stressors were without effect. Pretreatment with the β-norepinephrine antagonist propranolol precluded the immunosuppression elicited by a stressor applied 96 h after inoculation, but did not affect the reduction of the PFC response elicited by a stressor applied 120 h after inoculation. It is suggested that several factors may contribute to stressor-provoked alterations of the immune response, and that the contribution of these factors vary over the course of an immune response being mounted.
Stephen Safe - One of the best experts on this subject based on the ideXlab platform.
-
halogenated aromatic hydrocarbon induced suppression of the Plaque Forming Cell response in b6c3f1 splenocytes cultured with allogenic mouse serum ah receptor structure activity relationships
Toxicology, 1995Co-Authors: N Harper, M Steinberg, J Thomsen, Stephen SafeAbstract:The immunsuppressive effects of halogenated aromatic hydrocarbons (HAHs) were investigated in B6C3F1 female mice and in mouse splenocytes cultured with allogenic mouse serum using the Mishell-Dutton model for in vitro immunization to trinitrophenyl-lipopolysaccharide (TNP-LPS). Exposure to 2,3,7,8-tetrachlorodibenzo-P-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 1,2,3,7,8-PeCDF, 1,3,6,8-tetrachlorodibenzofuran (TCDF), 3,3′,4,4′,5-pentachlorobiphenyl (pentaCB), or 3,3′,4,4′,5,5′-hexaCB resulted in a dose-dependent suppression of the splenic Plaque-Forming Cell (PFC) response both in vivo and in vitro. The effective dose required to decrease 50% (ED50) of the response to 2,3,7,8-TCDD, 2,3,4,7,8-PeCDF, 1,2,3,7,8-PeCDF, 1,3,6,8-TCDF, 3,3′,4,4′,5-pentaCB, or 3,3′,4,4′,5,5′-hexaCB in vivo was 14.1, 5.5, 1695, 34800, 21, and 19 nmol/kg, respectively, and in vitro was 7.0, 10.6, 149, 2325, 9.1 and 9.1 nM, respectively. There was an exCellent rank order and linear correlation between the in vivo versus in vitro activities for these HAHs (r < 0.99) and the relative immunosuppressive potencies of these compounds paralleled their binding affinities for the aryl hydrocarbon (Ah) receptor. These results show that splenocytes cultured with allogenic mouse serum is an Ah-responsive in vitro assay which can be used for quantitating the immunosup-pressive effects of HAHS.
-
halogenated aryl hydrocarbon induced suppression of the in vitro Plaque Forming Cell response to sheep red blood Cells is not dependent on the ah receptor
Immunopharmacology, 1991Co-Authors: D Davis, Stephen SafeAbstract:Abstract The immunosuppressive effects of the halogenated aromatic hydrocarbons (HAHs), 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,9-PeCDF and 1,3,6,8-TCDF were investigated utilising the Mishell-Dutton model for in vitro immunization. The selected polychlorinated dibenzofuran congeners and 2,3,7,8-TCDD caused a concentration-dependent suppression of the splenic Plaque-Forming Cell response to sheep red blood Cells using Cell cultures derived from C57BL/6 (Ah responsive) mice. Previous studies showed that there was up to a 14900-fold difference in the in vivo immunotoxicity of these compounds, however in the in vitro studies, their immunosuppressive potencies were comparable. In addition, these congeners also exhibited similar potencies using spleen Cell cultures from DBA/2 (Ah-nonresponsive) mice. Previous research demonstrated that α-naphthoflavone was relatively inactive in the in vitro splenic assay system and that co-treatment of Cells from C57BL/6 mice with α-naphthoflavone (10 μM) plus 2,3,7,8-TCDD (20 mM) resulted in a significant inhibition of the immunotoxicity of 2,3,7,8-TCDD. In these studies, comparable interactive effects were also observed in Cells treated with α-naphthoflavone plus 1,3,6,8-TCDF, a weak in vivo Ah receptor agonist. Collectively, the results from this study suggest that there may be mechanism(s) of action for HAH-induced suppression of the in vitro murine humoral response to sheep red blood Cells which are independent of the Ah receptor protein.
M Tamura - One of the best experts on this subject based on the ideXlab platform.
-
modulation of the in vivo immune response by selective depletion of neutrophils using a monoclonal antibody rp 3 iii enhancement by rp 3 treatment of the anti sheep red blood Cell Plaque Forming Cell response in rats
Journal of Immunology, 1994Co-Authors: M Tamura, S Sekiya, M Terashita, F SendoAbstract:Because recent work has shown that neutrophils produce various cytokines and are activated by these agents, this study was undertaken to examine neutrophil participation in immune networks. In our previous work, we demonstrated that delayed type hypersensitivity to SRBC and accompanying mononuclear leukocyte recruitment are inhibited in vivo by selective depletion of neutrophils using a mAb designated RP-3. To elucidate the function of these Cells in Ab production, we assessed the splenic Plaque-Forming Cell response to SRBC in a rat model through selective depletion of circulating neutrophils by RP-3. This depletion which occurred at the time of immunization resulted in an increase in the number of anti-SRBC Ab producing Cells, as determined by the direct and indirect Plaque-Forming Cell response. This phenomenon was observed only when the Ag was administered i.p. and not with i.v. immunization. These results suggest that neutrophils suppress Ab production in certain situations.