| Modulation of Immunoglobulin Production by Invariant Vα19-Jα33 TCR-Bearing Cells. | |
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MedLine Citation:
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PMID: 21698203 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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We have previously shown that invariant Vα19-Jα33 TCR(+) (Vα19i T) cells suppress the disease progress in some models for organ specific autoimmune diseases and type IV allergy that deteriorate along with decline to excess in Th1- or Th17- immunity. In this study, we examined the effects of over-generation of Vα19i T cells on the Th2-controlled immunoglobulin isotype production in the models for type I allergy. IgE production by invariant Vα19-Jα33 TCR transgenic (Tg) mice was suppressed compared with that by non-Tg controls following administration with goat anti-mouse IgD antiserum or OVA, while IgG2a production was not influenced by the introduction of the transgene into the recipients. IgE production by wild type mice was similarly reduced when they were subjected to adoptive transfer with invariant Vα19-Jα33 TCR Tg(+) but not Tg(-) cells prior to immunization. Furthermore, the suppression of IgE production by these recipients was enhanced when they were previously administered with a Vα19i T cell activator, one of the modified α-mannosyl ceramides. In summary, it is suggested that Vα19i T cells have potential to participate in the homeostasis of immunity and that they suppress disease progression resulting from not only Th1- but also Th2- immunity excess. |
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Authors:
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Michio Shimamura; Yi-Ying Huang; Hiroshi Hidaka |
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Publication Detail:
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Type: Journal Article Date: 2011-06-16 |
Journal Detail:
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Title: PloS one Volume: 6 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2011 |
Date Detail:
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Created Date: 2011-06-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e20915 Citation Subset: IM |
Affiliation:
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Tsukuba Research Center for Interdisciplinary Materials Science and Graduate School of Pure and Applied Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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