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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 228 (1970), S. 1326-1327 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The mechanism of allogeneic inhibition remains obscure. Hellstrom et al.1 and Moller8 proposed that the in vitro 'cytotoxic effect of normal Fl hybrid lymphoid cells on parental type target cells, and growth inhibition in vivo, was caused by target cell confrontation with foreign isoantigens. ...
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In a previous report the authors demonstrated that acute graft-versus-host disease (GVHD) was associated with pathologic amounts of tumour necrosis factor alpha (TNF-α) and the appearance of lipopolysaccharide (LPS) in the blood of GVH reactive mice just prior to death. In this study the authors have investigated the kinetics of LPS accumulation in different organs during the course of acute GVHD using a murine model. Unirradiated C57BL/6×AF1 (B6AF1) mice were transplanted with C57BL/6 (B6) lymphoid cells and killed at predetermined times after transplantation for LPS analysis. Control animals were injected with either 60×106 B6AF1 lymphoid cells (syngeneic) or 60×106 irradiated (2000 rad) CBA lymphoid cells (allogeneic). Lipopolysaccharide began to appear in the liver and the spleen of GVH reactive mice from day 2 post-transplant and by day 10 all GVH reactive mice tested positive for hepatic and splenic LPS. Low levels of LPS were detected in some control mice from days 2 to 10 post-transplant but LPS was never detected after day 10 in control groups. Total hepatic and splenic LPS in acute GVH reactive mice peaked at a time coincident with the appearance of LPS in the serum and with the onset of mortality. These results demonstrate that tissue levels of LPS increase throughout the course of acute GVHD and are sufficient to trigger the release of pathologic amounts of TNF-α from primed macrophages resulting in the cachexia and mortality associated with acute GVHD in this model.
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  • 3
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In previous studies we demonstrated that an induced asialo-GMI positive (ASGMI+) cell of donor origin that exerts natural killer cell-like activity (NK activity+) plays a crucial role in the development of graft-versus-host (GVH)-associated tissue damage and severe immunosuppression. This study examined whether the ASGMI+ (NK activity+) GVH effector cells were activated by non-specific signals or whether these cells were triggered by specific alloantigens and displayed antigenic specificity, C57B1/6 (B6) donor mice were treated with either B6xAF1 (B6AF1) lymphoid cells and anti-asialo GM 1 antibodies (anti-ASGM I) to induce and eliminate specifically activated B6–anti-B6AF1 ASGM1+ (NK activity’(cells or with polyinosinic: ploycytidylic acid (poly I:C), and anti-ASGMI to eliminate non-specifically activated ASGM1+ (NK activity +) cells. Donor spleen and lymph node cells depleted of the specific allo-induced ASGMI+ NK reactive cells showed near normal numbers of L3T4+ and Lyt-2+ cells and retained T- and B-cell functions as measured by mitogen responses (to PHA. Con A and LPS). mixed lymphocyte responses (MLR) (to B6Ar'i)and the generation of cytotoxic T cells (CTL) (to B6AF1 blasts). Anti-ASGMI treatment almost completely abrogated NK activity in all donor inocula. GVH reactions were induced by injecting treated donor cells into B6AF1. B6 × C3HejF1 (B6C3HF1) and B6 x SJLF1 (B6SJLF1) hybrids and monitored by splenomegaly, suppression of T-cell mitogen responses and the development of histopathological lesions in the thymus. liver and pancreas. Cells from donors depleted of non-specifically (poly 1:C) induced ASGMI+ cells induced severe histological lesions, marked immunosuppression and splenomegaly in all three F| hybrid combinations. When the donor cells were depleted of specifically induced (B6–anti-B6AF1) ASGMI+ cells and injected into the three F1 combinations they induced splenomegaly in all three but caused severe tissue injury and intense immunosuppression only in B6C3HF1 and B6SJLF1 mice and not in B6AF1, mice. Genetic analysis suggests that the H-2D (or a closely related) region of the H-2 complex plays an important role in the activation of the specific GVH effector cells. These results suggest that the cell(s) responsible for splenomegaly are different from the ones that cause severe GVH-associated tissue damage and immunosuppression although there may be cells and/or lymphokines common to both processes GVH-associated tissue injury appears to be due to the induction of an effector cell that expresses ASGMI and exerts both NK-cell activity and specific cytotoxicity but does not appear to be from the T-cell population that is responsible for specific MLR and CTL activities in vitro.
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  • 4
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In vitro experiments were carried out to investigate the immunosuppressive effect of different populations of spleen cells obtained from animals experiencing a graft-versus-host reaction (GVHR). To induce the GVHR, parental lymphoid tells were injected into adult F1 hybrid mice. GVHR-activated spleen cells (GVH-SC) taken at different limes post-GVHR induction were separated into adherent and non-adherent fractions and treated with anti-θ serum plus complement. The different types of GVH-SC were added to either parental (donor-type) or F1 (host-type) normal spleen cells and cultured with sheep erythrocytes in a modified Marbrook chamber. It was found that both adherent and non-adherent 10-day GVH-SC significantly inhibited the plaque-forming cell response of F1 normal spleen cells hut not that of parental normal spleen cells. Significant suppression of the parental response was observed following the addition of 15-day GVH-SC or anti-θ treated adherent and non-adherent 7-day GVH-SC The results suggest that the non-specific immunosuppressive effect of GVH-SC is media led by GVHR-activated macrophages and B lymphocytes found in the anti-θ treated adherent and non-adherent fractions of the GVH-SC suspensions respectively.
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  • 5
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We investigated the association of peri-operative myocardial ischaemia with activation of coagulation and endogenous fibrinolysis in patients undergoing vascular surgery. In 50 patients, continuous Holter monitoring was performed to assess peri-operative myocardial ischaemia and 12-lead electrocardiography was recorded preoperatively and 72 h postoperatively to assess myocardial infarction. Serial blood samples were drawn peri-operatively to determine the concentrations of fibrin monomers (for activation of coagulation), d-dimer (for endogenous fibrinolysis) and cardiac troponin T and I. Patients with myocardial ischaemia showed higher concentrations of fibrin monomers at 48 h, and higher concentrations of d-dimer preoperatively and at 24 and 48 h postoperatively. In patients with peri-operative myocardial ischaemia, strong positive correlations were observed between fibrin monomer and d-dimer concentrations at 15 min and 4 h postoperatively, and cardiac troponins at 15 min and at 4, 24, 48 and 72 h postoperatively. Early postoperative activation of coagulation and fibrinolysis is associated with peri-operative myocardial cell damage among patients who are at risk for, or have a history of, coronary artery disease plus peri-operative myocardial ischaemia.
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