Abstract
In mice with hapten-induced CH, T cells of the CD4+ and CD8+ phenotypes activated the gene for JE, whereas CD8+ T cells alone caused activation of the gene for IP-10. In animals tolerized by feeding either TNCB or OX, hapten-induced expression of IP-10 but not JE mRNA was lost. The down-regulation of IP-10 gene activation was adoptively transferred from tolerized mice to naive mice by CD4+ splenic T cells. These findings reflect the differential roles of individual T-cell subsets in both enhancing and diminishing chemokine gene expression in contact hypersensitivity reactions.
MeSH terms
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Administration, Oral
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Administration, Topical
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Animals
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CD4-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / immunology
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Chemokines / biosynthesis*
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Dermatitis, Contact*
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Ear
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Gene Expression Regulation / immunology*
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Haptens
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Immune Tolerance*
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Mice
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Oxazolone / administration & dosage
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Oxazolone / immunology*
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Picryl Chloride / administration & dosage
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Picryl Chloride / immunology*
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RNA, Messenger / analysis
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RNA, Messenger / biosynthesis
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Skin / immunology
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Spleen / immunology
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T-Lymphocytes / immunology*
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Transcriptional Activation
Substances
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Chemokines
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Haptens
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RNA, Messenger
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Oxazolone
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Picryl Chloride