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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2004-2-9
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pubmed:abstractText |
A CIITA-independent pathway of MHC class II expression has been found in the eye and the brain, both immune-privileged sites. Although corneal endothelial cells were unable to express MHC class II in response to IFN-gamma alone, these cells readily expressed MHC class II molecules via a CIITA-independent pathway when triggered by simultaneous exposure to IFN-gamma and TNF-alpha. CIITA-independent expression of MHCclass II molecules enabled corneal endothelial cells to present cytosolic, but not endosomal, ovalbumin (OVA) to OVA-primed T cells. To determine whether CIITA-independent expression of MHC class II is relevant in vivo, minor H-only-incompatible corneal allografts prepared from CIITA knockout (KO) mice, MHC class II KO mice or wild-type donors were placed in eyes of normal mice. Cornea allografts from wild-type and CIITA KO mice suffered similar rejection fates, whereas far fewer class II-deficient corneas were rejected. In addition, MHC class II-bearing macrophages were observed in cuprizone-induced inflammatory and demyelinating brain lesions of CIITA KO mice. We conclude that class II expression via the CIITA-independent pathway enhances the vulnerability to rejection of corneal grafts expressing minor antigens. The potential relevance of CIITA-independent MHC class II expression at immune-privileged sites is discussed in relation to tolerance to strong autoantigens.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/H antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/MHC class II transactivator protein,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/invariant chain
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
471-80
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:14768052-Animals,
pubmed-meshheading:14768052-Antigens, Bacterial,
pubmed-meshheading:14768052-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:14768052-Brain,
pubmed-meshheading:14768052-Cornea,
pubmed-meshheading:14768052-Corneal Transplantation,
pubmed-meshheading:14768052-Endothelial Cells,
pubmed-meshheading:14768052-Endothelium,
pubmed-meshheading:14768052-Flow Cytometry,
pubmed-meshheading:14768052-Genes, MHC Class II,
pubmed-meshheading:14768052-Histocompatibility Antigens Class II,
pubmed-meshheading:14768052-Interferon-gamma,
pubmed-meshheading:14768052-Interleukin-2,
pubmed-meshheading:14768052-Male,
pubmed-meshheading:14768052-Mice,
pubmed-meshheading:14768052-Mice, Inbred BALB C,
pubmed-meshheading:14768052-Mice, Inbred C57BL,
pubmed-meshheading:14768052-Mice, Knockout,
pubmed-meshheading:14768052-Nuclear Proteins,
pubmed-meshheading:14768052-Trans-Activators,
pubmed-meshheading:14768052-Transcription, Genetic,
pubmed-meshheading:14768052-Tumor Necrosis Factor-alpha,
pubmed-meshheading:14768052-Up-Regulation
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pubmed:year |
2004
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pubmed:articleTitle |
A CIITA-independent pathway that promotes expression of endogenous rather than exogenous peptides in immune-privileged sites.
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pubmed:affiliation |
Schepens Eye Research Institute, Harvard Medical School, Boston, USA. arancibia@rics.bwh.harvard.edu
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pubmed:publicationType |
Journal Article
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