Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
1991-12-26
pubmed:abstractText
The role of major histocompatibility complex (MHC) class I expression in control of the sensitivity of normal cells to natural killer (NK) cells was studied by the use of mutant mice made deficient for expression of beta 2-microglobulin (beta 2m) through homologous recombination in embryonal stem cells. T-cell blasts from beta 2m-deficient (beta 2m -/-) mice were killed by NK cells from normal mice in vitro, while beta 2m +/- blasts were resistant. The beta 2m defect also affected the NK effector cell repertoire: NK cells from beta 2m -/- mice failed to kill beta 2m -/- blasts, while they retained the ability to kill the prototype NK cell target lymphoma YAC-1, although at reduced levels. The inability to recognize beta 2m -/- blasts could be transferred with beta 2m -/- bone marrow to irradiated beta 2m-expressing mice. In contrast, the development of CD8+ T cells (deficient in beta 2m -/- mice) was restored in such chimera. These results indicate that loss of MHC class I/beta 2m expression is sufficient to render normal cells sensitive to NK cells, and that the same defect in the hemopoietic system of a mouse renders its NK cells tolerant to beta 2m-deficient but otherwise normal cells. In the beta 2m -/- mice, NK cells may be selected or educated by other bone marrow cells to tolerate the MHC class I deficiency. Alternatively, the specificity may be controlled directly by the class I molecules on the NK cells themselves.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1694227, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1825103, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1853205, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1856626, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1979875, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-1987491, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2021423, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2112266, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2113557, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2139497, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2201309, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2654290, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2664068, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2682666, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2685607, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2814488, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-2970593, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-3171481, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-3549904, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-3584981, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-3951539, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-4942407, http://linkedlifedata.com/resource/pubmed/commentcorrection/1946452-593386
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10332-6
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Recognition of beta 2-microglobulin-negative (beta 2m-) T-cell blasts by natural killer cells from normal but not from beta 2m- mice: nonresponsiveness controlled by beta 2m- bone marrow in chimeric mice.
pubmed:affiliation
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't