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Article: Dendritic cells and oral transmission of prion diseases

TitleDendritic cells and oral transmission of prion diseases
Authors
KeywordsDendritic cells
Prion
TSE
Scrapie
Oral transmission
Issue Date2004
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/addr
Citation
Advanced Drug Delivery Reviews, 2004, v. 56 n. 6, p. 901-913 How to Cite?
AbstractAbstract Transmissible spongiform encephalopathies (scrapie, BSE, Kuru) develop as central nervous system (CNS) diseases after long incubation periods, and many of which may arise following the consumption of infected material. The infectious agent is thought to be a misfolded form (scrapie associated PrP (PrPSc)) of a normal host protein (cellular isoform of PrP (PrPC)), which is relatively resistant to proteolytic degradation and which serves as a template, directing host prion protein (PrP) to accumulate in the misfolded form. Animal experiments have shown that CNS disease is preceded by a period in which the agent accumulates in secondary lymphoid organs (Peyer's patches (PP), lymph nodes, spleen), particularly follicular dendritic cells (FDCs) in the B cell areas of these organs. How the agent is transmitted from the intestinal lumen to the FDCs is largely unknown. Dendritic cells (DCs, cells quite distinct from FDCs) are cells that are specialised to acquire antigens from peripheral tissues and to transport them to secondary lymphoid organs for presentation to T and B lymphocytes. We have shown that DCs can acquire PrPSc from the intestinal lumen and deliver it to mesenteric lymph nodes. In this review we discuss the different stages involved in the migration of PrPSc from the intestine to FDCs and consider the different stages and barriers involved in this process. We conclude that transport of the causative agent, using PrPSc as a biomarker, from the intestine to FDCs is a very inefficient process, which may help to account for the apparent low frequency of individuals who have consumed infected material that go on to develop clinical disease.
Persistent Identifierhttp://hdl.handle.net/10722/48654
ISSN
2015 Impact Factor: 15.606
2015 SCImago Journal Rankings: 5.200
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, FPen_HK
dc.contributor.authorMacPherson, GGen_HK
dc.date.accessioned2008-05-22T04:20:20Z-
dc.date.available2008-05-22T04:20:20Z-
dc.date.issued2004en_HK
dc.identifier.citationAdvanced Drug Delivery Reviews, 2004, v. 56 n. 6, p. 901-913en_HK
dc.identifier.issn0169-409Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/48654-
dc.description.abstractAbstract Transmissible spongiform encephalopathies (scrapie, BSE, Kuru) develop as central nervous system (CNS) diseases after long incubation periods, and many of which may arise following the consumption of infected material. The infectious agent is thought to be a misfolded form (scrapie associated PrP (PrPSc)) of a normal host protein (cellular isoform of PrP (PrPC)), which is relatively resistant to proteolytic degradation and which serves as a template, directing host prion protein (PrP) to accumulate in the misfolded form. Animal experiments have shown that CNS disease is preceded by a period in which the agent accumulates in secondary lymphoid organs (Peyer's patches (PP), lymph nodes, spleen), particularly follicular dendritic cells (FDCs) in the B cell areas of these organs. How the agent is transmitted from the intestinal lumen to the FDCs is largely unknown. Dendritic cells (DCs, cells quite distinct from FDCs) are cells that are specialised to acquire antigens from peripheral tissues and to transport them to secondary lymphoid organs for presentation to T and B lymphocytes. We have shown that DCs can acquire PrPSc from the intestinal lumen and deliver it to mesenteric lymph nodes. In this review we discuss the different stages involved in the migration of PrPSc from the intestine to FDCs and consider the different stages and barriers involved in this process. We conclude that transport of the causative agent, using PrPSc as a biomarker, from the intestine to FDCs is a very inefficient process, which may help to account for the apparent low frequency of individuals who have consumed infected material that go on to develop clinical disease.en_HK
dc.format.extent425393 bytes-
dc.format.extent657705 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/addren_HK
dc.rightsAdvanced Drug Delivery Reviews. Copyright © Elsevier BV.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectDendritic cellsen_HK
dc.subjectPrionen_HK
dc.subjectTSEen_HK
dc.subjectScrapieen_HK
dc.subjectOral transmissionen_HK
dc.titleDendritic cells and oral transmission of prion diseasesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0169-409X&volume=56&issue=6&spage=901&epage=913 &date=2004&atitle=Dendritic+cells+and+oral+transmission+of+prion+diseasesen_HK
dc.identifier.emailHuang, FP: fphuang@hkucc.hku.hken_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1016/j.addr.2003.09.006en_HK
dc.identifier.pmid15063597en_HK
dc.identifier.scopuseid_2-s2.0-1942504192-
dc.identifier.hkuros86120-
dc.identifier.isiWOS:000221131300013-

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