scholarly journals Hybrid Resistance Units

2020 ◽  
Author(s):  
Keyword(s):  
Hybrid Resistance

scholarly journals NK Cells Can Trigger Allograft Vasculopathy: The Role of Hybrid Resistance in Solid Organ Allografts

2005 ◽  
Vol 175 (5) ◽  
pp. 3424-3430 ◽  
Author(s):  
Shuichiro Uehara ◽  
Catharine M. Chase ◽  
William H. Kitchens ◽  
Harris S. Rose ◽  
Robert B. Colvin ◽  
...  
Keyword(s):  
Nk Cells ◽  
Solid Organ ◽  
Allograft Vasculopathy ◽  
Hybrid Resistance

Hybrid resistance against a natural killer (NK) cell-resistant lymphoma (YWA) is mediated by a T cell-dependent mechanism

1982 ◽  
Vol 18 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Alvar Grönberg ◽  
Gunnar O. Klein ◽  
Klas Kärre ◽  
Rolf Kiessling ◽  
George Klein
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Nk Cell ◽  
Hybrid Resistance ◽  
Dependent Mechanism

scholarly journals Murine Hertwig's anemia: premature death after normal bone marrow transplantation is radiation dose-dependent

Blood ◽  
1995 ◽  
Vol 85 (9) ◽  
pp. 2627-2631 ◽  
Author(s):  
JE Barker
Keyword(s):  
Radiation Dose ◽  
Radiation Damage ◽  
Marrow Transplantation ◽  
Premature Death ◽  
Mutant Mice ◽  
F1 Hybrid ◽  
Parental Type ◽  
Hybrid Resistance ◽  
Dose Dependent ◽  
Transplantation Therapy

Marrow transplantation therapy in mice with heritable blood disorders usually leads to rapid blood cell normalization, but is sometimes followed by pancytopenia and premature death. This is especially true in mice with Hertwig's anemia (an/an). Unlike the +/+ recipients, 100% of whom survive for over a year, 66% of the mutant mice die by 6 months posttransplantation, and the rest die soon thereafter. It is not clear whether premature death is due to the radiation dose (10 Gy) or to the fact that the F1 mutant mice receive parental-type cells known to induce hybrid resistance. In the present report, experiments were designed to determine whether the F1-an/an host is more sensitive to radiation and/or resistant to continued expansion of the parental-type +/+ cells. The mutant mice are, indeed, more sensitive to irradiation, with an LD100/30 of 7 Gy as compared with an LD100/30 of 10 Gy for the +/+ mice. The times of anemia onset and death for mutant mice implanted with +/+ cells postirradiation is also radiation dose-dependent. Further evidence that death is due to host radiation damage rather than F1 hybrid resistance was provided by transplanting cells from three morbid 10 Gy-irradiation recipients into unirradiated, anemic, stem cell-deficient, F1-W/Wv secondary hosts. All recipients were repopulated by the original parental cells, were cured of their anemia, and survived for 52 weeks posttransplantation. The an/an mouse's heightened susceptibility to radiation damage appears to be the major factor in early death after transplantation therapy.

scholarly journals The role of granzyme B in murine models of acute graft-versus-host disease and graft rejection

Blood ◽  
1996 ◽  
Vol 87 (4) ◽  
pp. 1232-1237 ◽  
Author(s):  
TA Graubert ◽  
JH Russell ◽  
TJ Ley
Keyword(s):  
Nk Cells ◽  
Graft Versus Host Disease ◽  
Graft Rejection ◽  
Granzyme B ◽  
Cytotoxic Lymphocytes ◽  
Host Disease ◽  
Graft Versus Host ◽  
Hybrid Resistance

A complete molecular description of the syndromes of graft-versus-host disease (GVHD) and graft rejection could have a significant impact on clinical bone marrow transplantation. Recent in vitro experiments (Heusel et al, Cell 76:977, 1994 and Shresta et al, Proc Natl Acad Sci USA 92:5679, 1995) have shown that the putative mediators of these two syndromes, cytotoxic lymphocytes (CTL) and natural killer (NK) cells, respectively, initiate a program of cell death (apoptosis) in susceptible target tissues in a manner critically dependent on the serine protease Granzyme B (gzm B). In the present study, we have analyzed the phenotype of gzm B-deficient mice using experimental transplant models designed to isolate their CD8+ CTL, CD4+ CTL, and NK compartments. We found a significant impairment in class I-dependent GVHD mediated by gzm B -/- CD8+ CTL, whereas class II-dependent GVHD was not altered using gzm B -/- CD4+ effectors. In a hybrid resistance model, gzm B -/- hosts rejected haplo-identical marrow grafts as efficiently as did their wild-type littermates. This result is surprising in light of a severe defect in the ability of gzm B -/- NK cells to induce apoptosis in susceptible targets in vitro. These in vivo data define significant role for gzm B in cytotoxicity mediated by CD8+ CTL, but not by CD4+ CTL. Furthermore, these results do not support a model of hybrid resistance in which NK cells play a pivotal role.

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