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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0005961,
umls-concept:C0014406,
umls-concept:C0022688,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0035015,
umls-concept:C0079189,
umls-concept:C0456387,
umls-concept:C1511636,
umls-concept:C1548437,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1882923,
umls-concept:C1947989
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pubmed:issue |
6
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pubmed:dateCreated |
1998-10-1
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pubmed:abstractText |
Mouse NK cells may use both cytokine, e.g. IFN-gamma, tumor necrosis factor (TNF)-alpha and IL-12, and cytotoxic, e.g. perforin and Fas-FasL, pathways to reject incompatible bone marrow cell (BMC) grafts. To begin a dissection of these two major pathways, mice bearing deletional mutations of IFN-gamma, TNF-RI/II or perforin, or mice treated with mAb to IL-12, IFN-gamma or NK1.1 were irradiated and challenged with class I-deficient BMC grafts, a system in which only NK cells are the effector cells. Proliferation of the donor-derived cells was judged in terms of splenic incorporation of [125I]iododeoxyuridine 5 or 7 days after cell transfer. All of these mice maintained in a specific pathogen-free (s.p.f.) environment were able to reject the BMC, except those treated with anti-NK1.1 mAb. However, perforin deficient mice maintained in a conventional breeding facility failed to reject class I (Tap-1)-deficient marrow cells. Transfer of mice from the pathogen-free to the conventional facility resulted in a slow and incomplete loss of the ability to reject marrow cells. Thus, the breeding colony environment can elicit otherwise undetectable defects in the rejection ability of perforin-deficient NK cells. This report will hopefully alert those investigators who have only studied immune gene knockout mice in s.p.f. facilities and found no significant abnormalities.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0953-8178
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
785-90
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9678759-Animals,
pubmed-meshheading:9678759-Antibodies, Monoclonal,
pubmed-meshheading:9678759-Bone Marrow Transplantation,
pubmed-meshheading:9678759-Cytokines,
pubmed-meshheading:9678759-Cytotoxins,
pubmed-meshheading:9678759-Environmental Exposure,
pubmed-meshheading:9678759-Graft Rejection,
pubmed-meshheading:9678759-Housing, Animal,
pubmed-meshheading:9678759-Killer Cells, Natural,
pubmed-meshheading:9678759-Mice,
pubmed-meshheading:9678759-Mice, Inbred C57BL,
pubmed-meshheading:9678759-Mice, Mutant Strains,
pubmed-meshheading:9678759-Specific Pathogen-Free Organisms
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pubmed:year |
1998
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pubmed:articleTitle |
Cytokine and cytotoxic pathways of NK cell rejection of class I-deficient bone marrow grafts: influence of mouse colony environment.
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pubmed:affiliation |
Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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