| Increase in CD230 (cellular prion protein) fluorescence on blood lymphocytes in bovine spongiform encephalopathy-infected nonhuman primates. | |
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MedLine Citation:
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PMID: 19843289 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The cellular prion protein (PrP(c)) plays a central role in prion diseases such as variant Creutzfeldt-Jakob disease. This disease can be transmitted by blood transfusion. However, the exact kinetics of blood infectivity and the blood fraction carrying infectivity have not yet been identified. STUDY DESIGN AND METHODS: Simian PrP(c) epitopes were mapped by flow cytometry using monoclonal antibodies (MoAbs). A whole blood/no wash protocol was established, validated, and applied to investigate peripheral blood cell-associated PrP(c) expression profiles in bovine spongiform encephalopathy (BSE)-infected cynomolgus monkeys and age-/sex-matched controls. In addition, physiologic expression patterns on blood cells and in lymphoid tissues were determined. RESULTS: In BSE-infected macaques, blood lymphocyte-associated PrP(c) fluorescence gradually increased years before the onset of clinical signs (p(F test) < 0.0001). The increase in fluorescence intensity was detectable with MoAb 12F10, whereas we failed to detect an increase with 3F4. In parallel, plasma concentrations of soluble CD230 also increased. Centrifugation of lymphocytes almost completely eliminated differences between infected and noninfected animals, most likely caused by a partial loss in cell-associated CD230 into the plasma supernatant. CONCLUSION: Blood lymphocytes from asymptomatically infected as well as diseased macaques were characterized by increased CD230 fluorescence, and phosphatidylinositol-phospholipase C-resistant PrP molecules contributed at least partially to this increase. Conformational changes within PrP(c) molecules may be the underlying mechanism for the increased PrP(c) fluorescence. This cell-associated phenomenon contributed at least partially to an increase in soluble plasma-derived PrP(c) levels. It is not yet known whether these changes reflect infectivity. |
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Authors:
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Edgar Holznagel; Barbara Yutzy; Walter Schulz-Schaeffer; Kay-Martin Hanschman; Andreas Stuke; Uwe Hahmann; Mechthild Törner; Cheick Coulibaly; Andreas Hoffmann; Gerhard Hunsmann; Johannes Löwer |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Validation Studies Date: 2009-10-15 |
Journal Detail:
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Title: Transfusion Volume: 50 ISSN: 1537-2995 ISO Abbreviation: Transfusion Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-03-17 Completed Date: 2010-03-30 Revised Date: 2010-11-16 |
Medline Journal Info:
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Nlm Unique ID: 0417360 Medline TA: Transfusion Country: United States |
Other Details:
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Languages: eng Pagination: 452-66 Citation Subset: IM |
Affiliation:
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Paul-Ehrlich-Institut, Federal Agency for Vaccines and Biomedicines, Langen, Germany. holed@pei.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Age Factors Animals Antibodies, Monoclonal / immunology Blood Preservation / methods Brain Cattle Encephalopathy, Bovine Spongiform / blood* Female Flow Cytometry Humans Immunophenotyping Injections Lymphocytes / chemistry* Lymphoid Tissue / chemistry Macaca fascicularis / blood* Mice Mice, Knockout Middle Aged PrPC Proteins / blood*, immunology Reproducibility of Results Specific Pathogen-Free Organisms Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/PrPC Proteins |
| Comments/Corrections | |
Comment In:
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Transfusion. 2010 Sep;50(9):2063-5; author reply 2065-6
[PMID:
21050226
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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