Increased resistance of (CBA x C57BL/6)F1 hybrids to the systemic graft versus host reaction during regeneration of the spleen

1979 ◽  
Vol 88 (5) ◽  
pp. 1330-1332
Author(s):  
R. Ya. Meshkova
Keyword(s):  
F1 Hybrids ◽  
Graft Versus Host Reaction ◽  
Host Reaction ◽  
Graft Versus Host ◽  
Regeneration Of The Spleen

scholarly journals Brief Report: Graft-Versus-Host Reaction in F1 Hybrid Mice Injected with Pre-Immunized Parental Thymus Cells

Blood ◽  
1964 ◽  
Vol 24 (6) ◽  
pp. 770-774 ◽  
Author(s):  
LUCIANO FIORE-DONATI ◽  
LUIGI CHIECO-BIANCHI ◽  
GIUSEPPE DE BENEDICTIS ◽  
GIUSEPPE TRIDENTE
Keyword(s):  
Lymphoid Cells ◽  
The Other ◽  
F1 Hybrids ◽  
Graft Versus Host Reaction ◽  
Host Reaction ◽  
F1 Hybrid ◽  
Graft Versus Host ◽  
Immunologic Activity ◽  
Thymus Cells ◽  
Hybrid Mice

Abstract Dissociated thymus cells are capable of initiating graft-versus-host reaction in (C3Hf/Gs x DBA/2)F1 hybrids only when derived from parental donors previously sensitized against the antigens of the other parental strain. The lower immunologic activity of thymus cells as compared with other lymphoid cells is presumably due to quantitative rather than qualitative differences in immunologically competent cells.

scholarly journals RAPID VIRAL INDUCTION OF MURINE LYMPHOMAS IN THE GRAFT-VERSUS-HOST REACTION

1972 ◽  
Vol 136 (6) ◽  
pp. 1533-1544 ◽  
Author(s):  
Eugene A. Cornelius
Keyword(s):  
F1 Hybrids ◽  
Graft Versus Host Reaction ◽  
Spleen Cells ◽  
Host Reaction ◽  
Tumor Induction ◽  
Susceptible Host ◽  
F1 Hybrid ◽  
Immunological Mechanism ◽  
Graft Versus Host ◽  
Induced Tumors

When weanling (SJL/J x C57BL/1)F1 hybrid mice were given five weekly-injections of small doses of viable SJL/J spleen cells, so as to induce a graft-versus-host reaction (GVHR), reticulum cell sarcomas were induced in all of the host mice by the 40th day after the first cell injection. Such tumors, on transplantation, were accepted by syngeneic (SJL/J x C57BL/1)F1 and C57BL/1 hosts, but not by SJL/J or NZB mice. Cell-free extracts of SJL/J spleens injected into similar hybrids resulted in identical tumors in all hosts within the same period; the transplantation characteristics were also similar. Normal (SJL/J x C57BL/1)F1 hybrids as well as similar hybrids injected with SJL/J liver or syngeneic F1 spleen cells did not develop tumors. Cell-free preparations of eight tumors induced in F1's by viable SLJ/J spleen cells were injected into newborn (C57BL/1 x A)F1 and C57BL/1 mice: tumors were induced, with seven of eight tumor preparations, with a latent period of 33–49 days. Such tumors were lymphosarcomas, and, in the case of (C57BL/1 x A)F1 hosts, further transplantation revealed that they were antigenically C57BL/1 tumors. These experiments provide conclusive evidence for a viral etiology of GVHR-induced tumors. Furthermore, tumor induction in the GVHR does not appear to depend specifically on an immunological mechanism but is most probably due to release or activation of a sufficient quantity of oncogenic virus within a certain time period in a highly susceptible host. Comparison with radiation induction of viral leukemia in mice revealed similarities in regard to optimal host age and the spacing of administration of the tumor-inducing agent. SJL/J mice carry a type C virus which causes a high incidence of spontaneous Hodgkin-like tumors by 1 yr of age; C57BL/1 mice do not develop lymphomas spontaneously but carry a latent leukemogenic virus. Their hybrid also has a low incidence of spontaneous lymphomas. Based on the results of these and previous experiments, the viruses of these strains of mice appear to be highly synergistic in tumor induction in the GVHR. The SJL/J virus is a powerful oncogenic agent. The C57BL/1 virus may be a helper virus to the SJL/J, but is a more powerful determinant of the antigenic composition of the induced tumors. This suggests that the virus of C57BL/1 mice, when activated, is capable of controlling the C57BL/1 genome. Because of the ease and rapidity of viral tumor induction, the SJL/J and C57BL/1 strains of mice, with their F1 hybrid, should be useful for further study of the mechanisms controlling induction of such tumors.

scholarly journals IMMUNOLOGIC INCOMPETENCE OF IMMUNOLOGICALLY RUNTED ANIMALS

1964 ◽  
Vol 119 (2) ◽  
pp. 211-224 ◽  
Author(s):  
R. Michael Blaese ◽  
Carlos Martinez ◽  
Robert A. Good
Keyword(s):  
Parent Strain ◽  
Neonatal Period ◽  
Lymphoid Cells ◽  
F1 Hybrids ◽  
Graft Versus Host Reaction ◽  
Spleen Cells ◽  
Host Reaction ◽  
Graft Versus Host ◽  
Donor Cells ◽  
C3h Mice

1. Adult (A x C57Bl/1)F1 hybrids regularly show runt disease when injected with adult spleen cells from A strain donors. This also occurs when A strain spleen cells are administered to adult C3H mice made tolerant of A strain tissue in the neonatal period. 2. Mice undergoing the graft versus host reaction fail to form antibodies to an intraperitoneal challenge of T2 bacteriophage. This phenomenon was observed well before any of the other overt signs of runting had occurred. Further, inhibition of antibody production to T2 phage by graft versus host reaction initiated at an interval following antigenic stimulation is demonstrated. 3. The basis for the immunologic incompetence of the host with respect to T2 phage is presumed to be the attack of immunologically competent donor cells on the lymphoid cells of the recipient. 4. The failure of the injected parent strain cells to respond to the antigen used may imply immunologic commitment of these cells.

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