Cell-based immunotherapy of prion diseases by adoptive transfer of antigen-loaded dendritic cells or antigen-primed CD4+ T lymphocytes
Identifieur interne : 001A56 ( Main/Exploration ); précédent : 001A55; suivant : 001A57Cell-based immunotherapy of prion diseases by adoptive transfer of antigen-loaded dendritic cells or antigen-primed CD4+ T lymphocytes
Auteurs : Claude Carnaud ; Véronique BachySource :
- Prion [ 1933-6896 ] ; 2010.
Abstract
Prion diseases are neurodegenerative conditions caused by the transconformation of a normal host glycoprotein, the cellular prion protein (PrPc) into a neurotoxic, self-aggregating conformer (PrPSc). TSEs are ineluctably fatal and no treatment is yet available. In principle, prion diseases could be attacked from different angles including: blocking conversion of PrPc into PrPSc, accelerating the clearance of amyloid deposits in peripheral tissues and brain, stopping prion progression in secondary lymphoid organs, reducing brain inflammation and promoting neuronal healing. There are many indications that adaptive and innate immunity might mediate those effects but, so far, the achievements of immunointervention have not matched all expectations. Difficulties arise from the impossibility to diagnose TSE before substantial brain damage, poor accessibility of the CNS to immunological agents, deep immune tolerance to self-PrP and short term effects of many immune interventions contrasting with the slow progression of TSEs. Here, we discuss two approaches, inspired from cancer immunotherapy, which might overcome some of those obstacles. One is vaccination with antigen-pulsed or antigen-transduced dendritic cells to bypass self-tolerance. The other one is the adoptive transfer of PrP-sensitized CD4+ T cells which can promote humoral, cellmediated or regulatory responses, coordinate adaptive and innate immunity and have long lasting effects.
Url:
PubMed: 20622507
PubMed Central: 2933053
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000326
- to stream Pmc, to step Curation: 000324
- to stream Pmc, to step Checkpoint: 000773
- to stream Ncbi, to step Merge: 000B78
- to stream Ncbi, to step Curation: 000B78
- to stream Ncbi, to step Checkpoint: 000B78
- to stream Main, to step Merge: 001B72
- to stream Main, to step Curation: 001A56
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cell-based immunotherapy of prion diseases by adoptive transfer of antigen-loaded dendritic cells or antigen-primed CD<sup>4+</sup>
T lymphocytes</title>
<author><name sortKey="Carnaud, Claude" sort="Carnaud, Claude" uniqKey="Carnaud C" first="Claude" last="Carnaud">Claude Carnaud</name>
</author>
<author><name sortKey="Bachy, Veronique" sort="Bachy, Veronique" uniqKey="Bachy V" first="Véronique" last="Bachy">Véronique Bachy</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">20622507</idno>
<idno type="pmc">2933053</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933053</idno>
<idno type="RBID">PMC:2933053</idno>
<date when="2010">2010</date>
<idno type="wicri:Area/Pmc/Corpus">000326</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000326</idno>
<idno type="wicri:Area/Pmc/Curation">000324</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000324</idno>
<idno type="wicri:Area/Pmc/Checkpoint">000773</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000773</idno>
<idno type="wicri:Area/Ncbi/Merge">000B78</idno>
<idno type="wicri:Area/Ncbi/Curation">000B78</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">000B78</idno>
<idno type="wicri:doubleKey">1933-6896:2010:Carnaud C:cell:based:immunotherapy</idno>
<idno type="wicri:Area/Main/Merge">001B72</idno>
<idno type="wicri:Area/Main/Curation">001A56</idno>
<idno type="wicri:Area/Main/Exploration">001A56</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cell-based immunotherapy of prion diseases by adoptive transfer of antigen-loaded dendritic cells or antigen-primed CD<sup>4+</sup>
T lymphocytes</title>
<author><name sortKey="Carnaud, Claude" sort="Carnaud, Claude" uniqKey="Carnaud C" first="Claude" last="Carnaud">Claude Carnaud</name>
</author>
<author><name sortKey="Bachy, Veronique" sort="Bachy, Veronique" uniqKey="Bachy V" first="Véronique" last="Bachy">Véronique Bachy</name>
</author>
</analytic>
<series><title level="j">Prion</title>
<idno type="ISSN">1933-6896</idno>
<idno type="eISSN">1933-690X</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Prion diseases are neurodegenerative conditions caused by the transconformation of a normal host glycoprotein, the cellular prion protein (PrPc) into a neurotoxic, self-aggregating conformer (PrPSc). TSEs are ineluctably fatal and no treatment is yet available. In principle, prion diseases could be attacked from different angles including: blocking conversion of PrPc into PrPSc, accelerating the clearance of amyloid deposits in peripheral tissues and brain, stopping prion progression in secondary lymphoid organs, reducing brain inflammation and promoting neuronal healing. There are many indications that adaptive and innate immunity might mediate those effects but, so far, the achievements of immunointervention have not matched all expectations. Difficulties arise from the impossibility to diagnose TSE before substantial brain damage, poor accessibility of the CNS to immunological agents, deep immune tolerance to self-PrP and short term effects of many immune interventions contrasting with the slow progression of TSEs. Here, we discuss two approaches, inspired from cancer immunotherapy, which might overcome some of those obstacles. One is vaccination with antigen-pulsed or antigen-transduced dendritic cells to bypass self-tolerance. The other one is the adoptive transfer of PrP-sensitized CD4<sup>+</sup>
T cells which can promote humoral, cellmediated or regulatory responses, coordinate adaptive and innate immunity and have long lasting effects.</p>
</div>
</front>
</TEI>
<affiliations><list></list>
<tree><noCountry><name sortKey="Bachy, Veronique" sort="Bachy, Veronique" uniqKey="Bachy V" first="Véronique" last="Bachy">Véronique Bachy</name>
<name sortKey="Carnaud, Claude" sort="Carnaud, Claude" uniqKey="Carnaud C" first="Claude" last="Carnaud">Claude Carnaud</name>
</noCountry>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001A56 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001A56 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= Main |étape= Exploration |type= RBID |clé= PMC:2933053 |texte= Cell-based immunotherapy of prion diseases by adoptive transfer of antigen-loaded dendritic cells or antigen-primed CD4+ T lymphocytes }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:20622507" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a ParkinsonFranceV1
![]() | This area was generated with Dilib version V0.6.29. | ![]() |