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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1992-7-27
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pubmed:abstractText |
Virally infected neurons avoid destruction by cytotoxic T lymphocytes (CTLs) by failing to express major histocompatibility complex (MHC) class I molecules. Like neurons in vivo and in primary culture, the OBL21 neuronal cell line expressed barely detectable levels of MHC class I molecules. This correlated with very low levels of mRNAs for the MHC class I heavy chains (alpha C). OBL21 cells also fail to provide MHC class I molecules with the peptides necessary for their efficient assembly and transport to the cell surface. This function can be restored by treatment with interferon-gamma (IFN-gamma). The mRNA for peptide transporters HAM1 and HAM2 was not detectable in OBL21 neuronal cells, but was induced by IFN-gamma treatment. Hence, the ability of neurons to evade CTL-mediated killing results from expression at low levels of the MHC class I alpha C, the peptide transporters HAM1 and HAM2, and possibly other genes of the peptide-loading machinery.
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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 |
0896-6273
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1185-90
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1610569-Animals,
pubmed-meshheading:1610569-Carrier Proteins,
pubmed-meshheading:1610569-Cell Line, Transformed,
pubmed-meshheading:1610569-Histocompatibility Antigens Class I,
pubmed-meshheading:1610569-Neurons,
pubmed-meshheading:1610569-Neuropeptides,
pubmed-meshheading:1610569-RNA, Messenger,
pubmed-meshheading:1610569-T-Lymphocytes, Cytotoxic
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pubmed:year |
1992
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pubmed:articleTitle |
Neuronal cells are deficient in loading peptides onto MHC class I molecules.
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pubmed:affiliation |
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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