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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1988-5-18
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pubmed:abstractText |
The MHC Ag expression on the surface of keratinocytes is altered after treatment with IFN. IFN-gamma induces, as expected, a strong increase in class I MHC Ag expression as well as de novo expression of class II MHC Ag, whereas IFN-alpha 2 only slightly increases class I MHC Ag and does not induce keratinocytes to express class II MHC Ag. We used untreated and IFN-pretreated keratinocytes as stimulators and also as targets to study whether IFN-induced MHC Ag changes would alter the immunogenicity of keratinocytes in alloimmune responses. It was found that class II MHC Ag-carrying keratinocytes were unable to induce the proliferation of resting lymphocytes, but did stimulate T blasts. Untreated keratinocytes were virtually resistant to the lysis by classical CTL but became susceptible after exposure to IFN-gamma, but not IFN-alpha 2 at physiologic doses. These data demonstrate mechanisms by which the release of IFN-gamma might contribute to the development of disease such as the graft vs host disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
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pubmed:volume |
140
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
2556-64
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2451691-Cell Division,
pubmed-meshheading:2451691-Cytotoxicity Tests, Immunologic,
pubmed-meshheading:2451691-Epidermis,
pubmed-meshheading:2451691-Gene Expression Regulation,
pubmed-meshheading:2451691-Histocompatibility Antigens,
pubmed-meshheading:2451691-Humans,
pubmed-meshheading:2451691-Immunologic Memory,
pubmed-meshheading:2451691-Interferons,
pubmed-meshheading:2451691-T-Lymphocytes, Cytotoxic
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pubmed:year |
1988
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pubmed:articleTitle |
IFN-mediated induction of MHC antigen expression on human keratinocytes and its influence on in vitro alloimmune responses.
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pubmed:affiliation |
Department of Internal Medicine, University of Innsbruck, Austria.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|