Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
|
| pubmed:dateCreated |
1997-3-10
|
| pubmed:abstractText |
Transplanted allogeneic marrow grafts often fail to engraft in a lethally irradiated host. Resistance to hemopoietic allograft is a complexed phenomenon involving multiple components. To study the involvement of a hemopoietic cytokine, which was known to play a role for stem cell function, we established lines of mice that were transgenic for human granulocyte colony-stimulating factor (hG-CSF). Elevated and constitutive expression was found in sera (1,041 +/- 242 pg/ml) of these transgenic mice regardless of their sexes and ages. Strong neutrophilic granulocytosis correlated with the elevated G-CSF activity in transgenic mice but not in littermate controls, establishing a functional expression of this cytokine. In lethally irradiated mice transgenic for G-CSF, infusion of fully allogeneic marrow cells induced donor-derived spleen colony. Growth of hemopoietic allografts appeared to be similar to those of syngeneic marrow cells, which indicates inhibition of resistance for allogeneic marrow grafts. Because of a positive correlation, involvement of natural killer (NK) cells in resistance of transplanted allografts has been suggested. Inocula of NK-sensitive lymphoma cells were, however, vigorously rejected in the G-CSF-transgenic mice. This observation indicates that G-CSF may play a role in engraftment of transplanted allogeneic marrow grafts and may represent a component of mechanisms of hemopoietic resistance. Furthermore, this result may be an indication that alloresistance and NK cells use different mechanisms to resist each target.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0160-564X
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
20
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
883-9
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8853800-Animals,
pubmed-meshheading:8853800-Base Sequence,
pubmed-meshheading:8853800-Bone Marrow Transplantation,
pubmed-meshheading:8853800-Female,
pubmed-meshheading:8853800-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:8853800-Graft Rejection,
pubmed-meshheading:8853800-Graft vs Host Reaction,
pubmed-meshheading:8853800-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:8853800-Hematopoiesis,
pubmed-meshheading:8853800-Humans,
pubmed-meshheading:8853800-Killer Cells, Natural,
pubmed-meshheading:8853800-Male,
pubmed-meshheading:8853800-Mice,
pubmed-meshheading:8853800-Mice, Inbred C57BL,
pubmed-meshheading:8853800-Mice, Transgenic,
pubmed-meshheading:8853800-Molecular Sequence Data,
pubmed-meshheading:8853800-Polymerase Chain Reaction,
pubmed-meshheading:8853800-Specific Pathogen-Free Organisms,
pubmed-meshheading:8853800-Stem Cells,
pubmed-meshheading:8853800-Transplantation, Homologous,
pubmed-meshheading:8853800-Tumor Cells, Cultured
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Selective inhibition of resistance to hemopoietic allografts but not rejection to a natural killer cell sensitive tumor in transgenic mice for granulocyte colony stimulating factor.
|
| pubmed:affiliation |
Department of Pathology, Sapporo Medical University, School of Medicine, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|