rdf:type |
|
lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0024518,
umls-concept:C0039195,
umls-concept:C0085358,
umls-concept:C0162388,
umls-concept:C0330390,
umls-concept:C0443288,
umls-concept:C0456387,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1706438,
umls-concept:C2698600
|
pubmed:issue |
23
|
pubmed:dateCreated |
1993-1-7
|
pubmed:abstractText |
Cytotoxic T lymphocytes (CTLs) recognize major histocompatibility complex (MHC) class I molecules, normally composed of a heavy chain, a beta 2-microglobulin (beta 2m), and peptide antigens. beta 2m is considered essential for the assembly and intracellular transport of MHC class I molecules as well as their peptide presentation to CTLs. Contrary to this dogma, we now report the generation of allospecific and restricted CD8+ and TCR alpha beta+ CTLs (where TCR is T-cell receptor) capable of killing beta 2m-deficient cells. Such CTLs were obtained by priming mice with live allogeneic beta 2m- spleen cells or mutant lymphoma cells producing MHC class I protein but no detectable beta 2m. Although both beta 2m- and beta 2m-expressing lymphoma cells were rejected in allogeneic mice, only the former were efficient inducers of CTLs recognizing beta 2m- cells. These CTLs were MHC class I (H-2Kb or Db)-specific and CD8-dependent and did not require serum as a source of external beta 2m in the culture. They could be induced across major and minor histocompatibility barriers. The H-2-restricted CTLs generated in the latter case failed to kill the antigen-processing-deficient target RMA-S cells. The results show that MHC class I heavy chains in beta 2m- cells can be transported to the cell surface and act as antigens or antigen-presenting molecules to allospecific and MHC-restricted CTLs.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1309852,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1311017,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1538753,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1546329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1557127,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1740666,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1758495,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1912514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1936122,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-1940788,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2032286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2034289,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2062379,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2112266,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2124002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2139497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2198471,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2318516,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2326647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2342577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2469442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2514106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2666863,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-2731965,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-3532114,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-3951539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1454824-77067
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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 |
Dec
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
89
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
11381-5
|
pubmed:dateRevised |
2010-9-7
|
pubmed:meshHeading |
pubmed-meshheading:1454824-Animals,
pubmed-meshheading:1454824-Antigens, CD8,
pubmed-meshheading:1454824-Cytotoxicity, Immunologic,
pubmed-meshheading:1454824-Histocompatibility Antigens Class I,
pubmed-meshheading:1454824-Major Histocompatibility Complex,
pubmed-meshheading:1454824-Mice,
pubmed-meshheading:1454824-Mice, Inbred Strains,
pubmed-meshheading:1454824-T-Lymphocyte Subsets,
pubmed-meshheading:1454824-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:1454824-beta 2-Microglobulin
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pubmed:year |
1992
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pubmed:articleTitle |
Major histocompatibility complex class I-specific and -restricted killing of beta 2-microglobulin-deficient cells by CD8+ cytotoxic T lymphocytes.
|
pubmed:affiliation |
Department of Tumor Biology, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|