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Holger W Hirte - One of the best experts on this subject based on the ideXlab platform.
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decidua associated Suppressor cells in abortion prone dba 2 mated cba j mice that release bioactive transforming growth Factor beta2 related immunosuppressive molecules express a bone marrow derived natural Suppressor cell marker and gamma delta t ce
Biology of Reproduction, 1997Co-Authors: David A Clark, Fatima S Merali, David W Hoskin, Darlene Steelnorwood, Petra C Arck, Kenneth Croitoru, Robert A Murgita, Holger W HirteAbstract:The decidua of allopregnant mice contains a novel population of Thyl- Lytl CD4- CD8- asialoGM1 non-B small lymphocytic Suppressor cells that release transforming growth Factor (TGF) 2-related Suppressor molecules. The "null" phenotype of this cell population is similar to some bone marrowderived natural Suppressor cell (NSC) populations, and the latter may release TGFfis. We now report that the TGFP2-producing Suppressor cells in the uterine decidua of DBA/2-mated CBA/J female mice-linked to prevention of abortions-are inactivated effectively by 1E5/B5.1 but not by 2C1.1 rat monoclonal antibodies to murine pregnancy-associated splenic NSC in the presence of complement. Immunostaining of a subpopulation of cells in decidua with 1E5/B5.1 but not with 2C1.1 was shown by flow cytometry. Release of Suppressor Factor was also abrogated by 1 E5/B5.1 + complement but not by 2C1.1 + complement, and the Suppressor Factor was specifically neutralized by anti-TGFI32 and not by anti-TGFI3. Splenic pregnancy NSC are susceptible to 2C1.1, produce TGFPI1, and express CD3 and ois T-cell receptor (TcR) chains. Release of Suppressor Factor by the decidual NSC was abrogated by treatment with anti-CD3 (145 2C11) and anti-TcR y86 (GL4) monoclonal antibodies + complement, but not by anti-TcR 4ap (H57) + complement; and cells sorted using anti-TcR y8 (GL3) released suppressive activity in vitro. Slightly more suppressive activity was released by implantation-site decidua where there was no epithelium than from epithelialized inter-implantation-site decidua; no significant activity was released from placental tissue, but combining implantation-site tissue with placental tissue led to release of enhanced levels of immunosuppressive activity. There appear to be subtypes of bone marrow-derived TcR + NSC with different phenotypes and tissue localization patterns in pregnancy. The previously reported dependence of decidual NSC activity on the presence of soluble signals from fetal trophoblast may be explainable by the ability of cells bearing TcR y8 to recognize and react to placental trophoblast cell antigen.
Konstantin -a. Hossmann - One of the best experts on this subject based on the ideXlab platform.
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The effect of global ischemia and recirculation of rat brain on protein synthesisin vitro
Metabolic Brain Disease, 1993Co-Authors: Gönül Erdogdu, Akira Uto, Konstantin -a. HossmannAbstract:Transient cerebral ischemia causes long-lasting inhibition of protein synthesis despite recovery of energy metabolism. We investigated the question if this inhibition is due to the formation of a suppression Factor which interferes with the function of the protein synthesizing machinery. For this purpose rats were submitted to 20 minutes four vessel-occlusion followed by recirculation times from 30 minutes to 7 days. Post-mitochondrial supernatant (PMS) from various brain regions was added to a self-contained, cell-free rabbit reticulocyte translational system, and the effect on in vitro protein synthesis was assessed by measuring^14C-leucine incorporation over a duration of 45 minutes. PMS prepared at the end of ischemia from hippocampus, striatum and cerebellum inhibited in vitro protein synthesis by 40%–60% but there was only a minor inhibition by PMS from cerebral cortex. During post-ischemic recirculation cortical PMS transiently induced inhibition of in vitro protein synthesis by 30% but this effect gradually disappeared within one week. The inhibition caused by PMS from hippocampus, striatum and cerebellum was not reversed during recirculation and still amounted to about 40% after 7 days. Inhibition of in vitro protein synthesis could be blocked by heating PMS to 100°C, indicating that the Suppressor Factor is a protein. The comparison of the in vitro effect of postischemic PMS with previously described in vivo inhibition of protein synthesis demonstrates that the here observed Suppressor Factor is not able to explain the overall disturbance of protein synthesis in vivo. However, the inhibitory potency of this Factor after as long as 7 days after recirculation points to an ongoing pathological process, the importance of which remains to be clarified.
David A Clark - One of the best experts on this subject based on the ideXlab platform.
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decidua associated Suppressor cells in abortion prone dba 2 mated cba j mice that release bioactive transforming growth Factor beta2 related immunosuppressive molecules express a bone marrow derived natural Suppressor cell marker and gamma delta t ce
Biology of Reproduction, 1997Co-Authors: David A Clark, Fatima S Merali, David W Hoskin, Darlene Steelnorwood, Petra C Arck, Kenneth Croitoru, Robert A Murgita, Holger W HirteAbstract:The decidua of allopregnant mice contains a novel population of Thyl- Lytl CD4- CD8- asialoGM1 non-B small lymphocytic Suppressor cells that release transforming growth Factor (TGF) 2-related Suppressor molecules. The "null" phenotype of this cell population is similar to some bone marrowderived natural Suppressor cell (NSC) populations, and the latter may release TGFfis. We now report that the TGFP2-producing Suppressor cells in the uterine decidua of DBA/2-mated CBA/J female mice-linked to prevention of abortions-are inactivated effectively by 1E5/B5.1 but not by 2C1.1 rat monoclonal antibodies to murine pregnancy-associated splenic NSC in the presence of complement. Immunostaining of a subpopulation of cells in decidua with 1E5/B5.1 but not with 2C1.1 was shown by flow cytometry. Release of Suppressor Factor was also abrogated by 1 E5/B5.1 + complement but not by 2C1.1 + complement, and the Suppressor Factor was specifically neutralized by anti-TGFI32 and not by anti-TGFI3. Splenic pregnancy NSC are susceptible to 2C1.1, produce TGFPI1, and express CD3 and ois T-cell receptor (TcR) chains. Release of Suppressor Factor by the decidual NSC was abrogated by treatment with anti-CD3 (145 2C11) and anti-TcR y86 (GL4) monoclonal antibodies + complement, but not by anti-TcR 4ap (H57) + complement; and cells sorted using anti-TcR y8 (GL3) released suppressive activity in vitro. Slightly more suppressive activity was released by implantation-site decidua where there was no epithelium than from epithelialized inter-implantation-site decidua; no significant activity was released from placental tissue, but combining implantation-site tissue with placental tissue led to release of enhanced levels of immunosuppressive activity. There appear to be subtypes of bone marrow-derived TcR + NSC with different phenotypes and tissue localization patterns in pregnancy. The previously reported dependence of decidual NSC activity on the presence of soluble signals from fetal trophoblast may be explainable by the ability of cells bearing TcR y8 to recognize and react to placental trophoblast cell antigen.
Thomas J. Rogers - One of the best experts on this subject based on the ideXlab platform.
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In vivo analysis of a superantigen-induced T cell Suppressor Factor.
Cellular Immunology, 1996Co-Authors: William K. Cornwell, Thomas J. Rogers, Yee Shin LinAbstract:Abstract We have previously reported that the superantigen staphylococcal enterotoxin B (SEB) was able to suppress an immune response to sheep red blood cells when administered intravenously to mice. While the capacity of the superantigens to stimulate lymphocytes and accessory cell functions has been thoroughly examined, it is clear that these agents may also exhibit potent immunosuppressive activity both in vivo and in vitro. This SEB-induced immunosuppression was determined by our laboratories to be mediated by a population of T Suppressor cells. The suppression may be due to the generation of inhibitory lymphokines, including IL-10 or transforming growth Factor β, following superantigen stimulation. Alternatively, the immunomodulatory activity may be due to the activation of antigen-specific and/or genetically restricted Suppressor cells by SEB. The mechanism of activity of these Suppressor cells has not been fully defined. In this report we wished to determine whether a Suppressor Factor generated from SEB-activated T cells in vitro may be responsible for the inhibition of antibody or delayed-type hypersensitivity responses in vivo. We observed that both antibody and delayed-type hypersensitivity responses were inhibited following administration of the SEB-induced Suppressor Factor. The in vivo inhibitory activity of the SEB-induced Suppressor Factor was found to be genetically restricted at the “I–J” locus. In addition, monoclonal anti-I–J antibodies recognized the Suppressor Factor in a haplotype-specific fashion. These results show that the suppressive product of SEB-induced T cells possesses the ability to inhibit, in a genetically restricted fashion, both cellular and humoral immune responses.
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Immunosuppressive activity of staphylococcal enterotoxin B. II. Activation of Suppressor-effector cells by a staphylococcal enterotoxin B-induced Suppressor Factor.
Cellular Immunology, 1990Co-Authors: Dennis D. Taub, Yee Shin Lin, Thomas J. RogersAbstract:Abstract The capacity of Staphylococcal enterotoxins to stimulate all T cells bearing certain T cell receptors has recently generated a great deal of interest. These toxins are believed to bind directly both to the TCR:CD4 complex via its Vβ domains and to class II MHC molecules on accessory cells prior to T cell activation. Previous studies from this laboratory have demonstrated that staphylococcal enterotoxin B (SEB) is capable of inducing multiple T Suppressor cell populations which can inhibit in vitro antibody responses. Additional studies have demonstrated that the suppressive activity of these cells is mediated, at least in part, by an I-J-restricted Suppressor Factor. Efforts to characterize the inhibitory activity of this Factor have demonstrated that the suppressive element is capable of activating both early and late acting Suppressor cell populations in vitro . Analysis by both positive and negative selection shows that cells bearing the Lyt1 − 2 + surface marker phenotype are active early, whereas Lyt1 + 2 + cells are active both early and late in the antibody response. Additional experiments using various strains of mice as sources of Suppressor Factor and of naive splenocyte populations have demonstrated that activation of Suppressor-effector cells by this Suppressor Factor is restricted at the I-J, but not Igh, gene locus. These studies suggest that this SEB-induced Suppressor Factor alone provides the signals necessary for the induction and activation of Suppressor-effector cell activity.
Yee Shin Lin - One of the best experts on this subject based on the ideXlab platform.
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In vivo analysis of a superantigen-induced T cell Suppressor Factor.
Cellular Immunology, 1996Co-Authors: William K. Cornwell, Thomas J. Rogers, Yee Shin LinAbstract:Abstract We have previously reported that the superantigen staphylococcal enterotoxin B (SEB) was able to suppress an immune response to sheep red blood cells when administered intravenously to mice. While the capacity of the superantigens to stimulate lymphocytes and accessory cell functions has been thoroughly examined, it is clear that these agents may also exhibit potent immunosuppressive activity both in vivo and in vitro. This SEB-induced immunosuppression was determined by our laboratories to be mediated by a population of T Suppressor cells. The suppression may be due to the generation of inhibitory lymphokines, including IL-10 or transforming growth Factor β, following superantigen stimulation. Alternatively, the immunomodulatory activity may be due to the activation of antigen-specific and/or genetically restricted Suppressor cells by SEB. The mechanism of activity of these Suppressor cells has not been fully defined. In this report we wished to determine whether a Suppressor Factor generated from SEB-activated T cells in vitro may be responsible for the inhibition of antibody or delayed-type hypersensitivity responses in vivo. We observed that both antibody and delayed-type hypersensitivity responses were inhibited following administration of the SEB-induced Suppressor Factor. The in vivo inhibitory activity of the SEB-induced Suppressor Factor was found to be genetically restricted at the “I–J” locus. In addition, monoclonal anti-I–J antibodies recognized the Suppressor Factor in a haplotype-specific fashion. These results show that the suppressive product of SEB-induced T cells possesses the ability to inhibit, in a genetically restricted fashion, both cellular and humoral immune responses.
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Immunosuppressive activity of staphylococcal enterotoxin B. II. Activation of Suppressor-effector cells by a staphylococcal enterotoxin B-induced Suppressor Factor.
Cellular Immunology, 1990Co-Authors: Dennis D. Taub, Yee Shin Lin, Thomas J. RogersAbstract:Abstract The capacity of Staphylococcal enterotoxins to stimulate all T cells bearing certain T cell receptors has recently generated a great deal of interest. These toxins are believed to bind directly both to the TCR:CD4 complex via its Vβ domains and to class II MHC molecules on accessory cells prior to T cell activation. Previous studies from this laboratory have demonstrated that staphylococcal enterotoxin B (SEB) is capable of inducing multiple T Suppressor cell populations which can inhibit in vitro antibody responses. Additional studies have demonstrated that the suppressive activity of these cells is mediated, at least in part, by an I-J-restricted Suppressor Factor. Efforts to characterize the inhibitory activity of this Factor have demonstrated that the suppressive element is capable of activating both early and late acting Suppressor cell populations in vitro . Analysis by both positive and negative selection shows that cells bearing the Lyt1 − 2 + surface marker phenotype are active early, whereas Lyt1 + 2 + cells are active both early and late in the antibody response. Additional experiments using various strains of mice as sources of Suppressor Factor and of naive splenocyte populations have demonstrated that activation of Suppressor-effector cells by this Suppressor Factor is restricted at the I-J, but not Igh, gene locus. These studies suggest that this SEB-induced Suppressor Factor alone provides the signals necessary for the induction and activation of Suppressor-effector cell activity.