Source:http://linkedlifedata.com/resource/pubmed/id/10823419
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2000-6-1
|
pubmed:abstractText |
We injected cyclophosphamide into mice and examined their natural killer (NK) activity both in vitro and in vivo. Cyclophosphamide injection temporarily abrogated the lung clearance activity of Yac-1 lymphoma cells, which is considered to be an index of NK activity in vivo. However, administration of recombinant human macrophage-colony-stimulating-factor (rhM-CSF) to cyclophosphamide-injected mice restored the lung clearance activity. To clarify whether the administration of rhM-CSF activated NK cells, we purified NK1.1+ cells from mice treated with cyclophosphamide and/or rhM-CSF and examined their functions (cytotoxicity, proliferation, and interferon gamma production) in vitro. Cyclophosphamide injection decreased the number, but did not suppress the functions of NK1.1+ cells. The numbers of NK1.1+ cells in cyclophosphamide-injected mice restored by rhM-CSF administration. And the functions of NK1.1+ cells from both saline-injected and cyclophosphamide-injected mice were accelerated by rhM-CSF administration. These results suggested that the temporary abrogation of NK activity in vivo caused by cyclophosphamide injection was due to a decrease in the number and not to suppression of the functions of NK1.1+ cells. The injection of cyclophosphamide into mice increased the number of tumor (B16 melanoma) nodules formed in the lungs and liver. However, treatment with rhM-CSF recovered the anti-metastatic activity in the lungs of cyclophosphamide-injected mice. These results show that administration of rhM-CSF restores NK activity suppressed by cyclophosphamide injection in vivo.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclophosphamide,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/KLRB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Klrb1c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Colony-Stimulating Factor,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0340-7004
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
49
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
94-100
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:10823419-Animals,
pubmed-meshheading:10823419-Antigens,
pubmed-meshheading:10823419-Antigens, Ly,
pubmed-meshheading:10823419-Antigens, Surface,
pubmed-meshheading:10823419-Cyclophosphamide,
pubmed-meshheading:10823419-Hematopoiesis,
pubmed-meshheading:10823419-Interferon-gamma,
pubmed-meshheading:10823419-Killer Cells, Natural,
pubmed-meshheading:10823419-Lectins, C-Type,
pubmed-meshheading:10823419-Lung Neoplasms,
pubmed-meshheading:10823419-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:10823419-Male,
pubmed-meshheading:10823419-Melanoma, Experimental,
pubmed-meshheading:10823419-Mice,
pubmed-meshheading:10823419-Mice, Inbred C57BL,
pubmed-meshheading:10823419-NK Cell Lectin-Like Receptor Subfamily B,
pubmed-meshheading:10823419-Proteins,
pubmed-meshheading:10823419-Recombinant Proteins
|
pubmed:year |
2000
|
pubmed:articleTitle |
Effects of macrophage-colony-stimulating factor on cyclophosphamide-injected mouse NK1.1+ cell activity.
|
pubmed:affiliation |
Biochemical Research Laboratory, Morinaga Milk Industry Co. Ltd., Zama City, Kanagawa pref., Japan.
|
pubmed:publicationType |
Journal Article
|