rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1-2
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pubmed:dateCreated |
2006-9-5
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pubmed:abstractText |
Activation of Th2 cells suppresses clinical experimental autoimmune encephalitis (EAE), demyelination and expression of genes associated with Th1-mediated inflammation. Despite both reduced central nervous system inflammation and IFN-gamma induced MHC class II expression by microglia, the composition of CNS infiltrates in Th2-protected mice were similar to mice with EAE. Analysis of the CNS infiltrating cells by flow cytometry suggests that protection did not correlate with abrogation of CD4+ T cell recruitment, preferential recruitment of donor Th2 cells or an increased frequency of CD25+ CD4+ T cells. By contrast, protection correlated with an increased frequency of neuroantigen-specific Th2 cells infiltrating the CNS. These data suggest that a peripheral Th2 cytokine environment influences both potential antigen presenting cells as well as recruitment and/or retention of neuroAg-specific Th2 CD4+ T cells.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hemocyanin,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Proteolipid Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Plp1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/keyhole-limpet hemocyanin
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0165-5728
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
30-9
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pubmed:dateRevised |
2008-7-9
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pubmed:meshHeading |
pubmed-meshheading:16814872-Adoptive Transfer,
pubmed-meshheading:16814872-Animals,
pubmed-meshheading:16814872-Antigens,
pubmed-meshheading:16814872-Cytokines,
pubmed-meshheading:16814872-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:16814872-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:16814872-Female,
pubmed-meshheading:16814872-Flow Cytometry,
pubmed-meshheading:16814872-Gene Expression,
pubmed-meshheading:16814872-Hemocyanin,
pubmed-meshheading:16814872-Histocompatibility Antigens Class II,
pubmed-meshheading:16814872-Lymphocyte Activation,
pubmed-meshheading:16814872-Male,
pubmed-meshheading:16814872-Mice,
pubmed-meshheading:16814872-Myelin Proteolipid Protein,
pubmed-meshheading:16814872-Nerve Tissue Proteins,
pubmed-meshheading:16814872-RNA, Messenger,
pubmed-meshheading:16814872-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16814872-Spinal Cord,
pubmed-meshheading:16814872-Th1 Cells,
pubmed-meshheading:16814872-Th2 Cells
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pubmed:year |
2006
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pubmed:articleTitle |
Altered neuroantigen-specific cytokine secretion in a Th2 environment reduces experimental autoimmune encephalomyelitis.
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pubmed:affiliation |
Department of Molecular Microbiology and Immunology, University of Southern California, Keck School of Medicine, 1333 San Pablo Ave, Los Angeles, CA 90033, USA.
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pubmed:publicationType |
Journal Article
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