TY - JOUR
T1 - Inhibition of resistance to hemopoietic allo-grafts in granulocyte colony-stimulating factor transgenic mice
AU - Kokai, Yasuo
AU - Kaneko, Hideo
AU - Izuka, Kooh
AU - Matsuura, Akihiro
AU - Fujimoto, Junichiro
PY - 1996/1
Y1 - 1996/1
N2 - Transplanted allogeneic marrow cells often fail to engraft in a lethally irradiated host. This phenomenon, termed resistance to allogeneic marrow grafts or allo-resistance, is well documented, although its mechanism is not yet understood. Transplantation of major histocompatibility complex disparate allogeneic marrow cells into mice transgenic for granulocyte colony-stimulating factor (G-CSF) showed donor-derived spleen colonies (CFU-S) and resulted in stable allogeneic chimerism with excellent survival (100% up to 40 days and 89% up to 120 days). Under the same experimental conditions, all the littermate controls failed to show CFU-S and died shortly after marrow transplantation. Thus, resistance to allogeneic marrow cells appeared to be severely impaired in this transgenic mouse. The observation that neutralizing antibody against G-CSF restored allo-resistance in G-CSF transgenic mice and that CFU-S was inducible upon administration of recombinant G-CSF using a mini-osmotic pump in nontransgenic recipients, suggests that an elevated level of this cytokine is important for the inhibition of allo-resistance. Thus, G-CSF was found to play a role in allogeneic resistance to marrow grafts and the G-CSF-transgenic mice provide a useful model to study the inhibition of the resistance. The inhibition of allo-resistance may be useful in preparing allogeneic bone marrow chimeras in both experimental and clinical settings.
AB - Transplanted allogeneic marrow cells often fail to engraft in a lethally irradiated host. This phenomenon, termed resistance to allogeneic marrow grafts or allo-resistance, is well documented, although its mechanism is not yet understood. Transplantation of major histocompatibility complex disparate allogeneic marrow cells into mice transgenic for granulocyte colony-stimulating factor (G-CSF) showed donor-derived spleen colonies (CFU-S) and resulted in stable allogeneic chimerism with excellent survival (100% up to 40 days and 89% up to 120 days). Under the same experimental conditions, all the littermate controls failed to show CFU-S and died shortly after marrow transplantation. Thus, resistance to allogeneic marrow cells appeared to be severely impaired in this transgenic mouse. The observation that neutralizing antibody against G-CSF restored allo-resistance in G-CSF transgenic mice and that CFU-S was inducible upon administration of recombinant G-CSF using a mini-osmotic pump in nontransgenic recipients, suggests that an elevated level of this cytokine is important for the inhibition of allo-resistance. Thus, G-CSF was found to play a role in allogeneic resistance to marrow grafts and the G-CSF-transgenic mice provide a useful model to study the inhibition of the resistance. The inhibition of allo-resistance may be useful in preparing allogeneic bone marrow chimeras in both experimental and clinical settings.
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U2 - 10.1002/eji.1830260118
DO - 10.1002/eji.1830260118
M3 - Article
C2 - 8566053
AN - SCOPUS:0030060328
SN - 0014-2980
VL - 26
SP - 115
EP - 119
JO - European Journal of Immunology
JF - European Journal of Immunology
IS - 1
ER -