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Francisella tularensis strain LVS resides in MHC II-positive autophagic vacuoles in macrophages
Roman Hrstka, Zuzana Kročová, J. Černý, Bořivoj Vojtěšek, Aleš Macela, Jiří Stulík
Jazyk angličtina Země Česko
PubMed
18450226
DOI
10.1007/bf02932193
Knihovny.cz E-zdroje
- MeSH
- buněčná smrt genetika imunologie MeSH
- cytosol fyziologie imunologie mikrobiologie MeSH
- financování organizované využití MeSH
- fluorescenční mikroskopie využití MeSH
- fosfohydroláza PTEN genetika imunologie izolace a purifikace MeSH
- Francisella tularensis imunologie izolace a purifikace MeSH
- imunoblotting metody využití MeSH
- kathepsin D genetika imunologie izolace a purifikace MeSH
- makrofágy imunologie mikrobiologie MeSH
- tularemie etiologie imunologie mikrobiologie MeSH
The Francisella tularensis strain LVS phagosome disintegrates during the first few hours after bacterial entry and microbes are released to the cytosol. Within 12 h both rapid multiplication of microbes and a steep increase of apoptosis of infected macrophages occur. We searched for signals involved in the death of macrophages and detected molecules associated with the autophagy machinery cathepsin D, PTEN, p53 and LC3, whose levels or modification were influenced by ongoing in vitro tularemic infection. The sequestration of cytoplasmic F. tularensis LVS into autophagosomes was confirmed by co-localization of the LVS strain containing vacuoles with LC3 (an autophagosomal marker). We also demonstrated the presence of MHC II antigens in these autophagosomes, indicating that they might act as a source of endogenous tularemic antigens for presentation to CD4+ T lymphocytes.
Citace poskytuje Crossref.org
Lit.: 27
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- $a The Francisella tularensis strain LVS phagosome disintegrates during the first few hours after bacterial entry and microbes are released to the cytosol. Within 12 h both rapid multiplication of microbes and a steep increase of apoptosis of infected macrophages occur. We searched for signals involved in the death of macrophages and detected molecules associated with the autophagy machinery cathepsin D, PTEN, p53 and LC3, whose levels or modification were influenced by ongoing in vitro tularemic infection. The sequestration of cytoplasmic F. tularensis LVS into autophagosomes was confirmed by co-localization of the LVS strain containing vacuoles with LC3 (an autophagosomal marker). We also demonstrated the presence of MHC II antigens in these autophagosomes, indicating that they might act as a source of endogenous tularemic antigens for presentation to CD4+ T lymphocytes.
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