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Oxidized lipids keep heat shock chaperones busy: new insights on the deficiencies of tumour-associated dendritic cells

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Published in Journal for ImmunoTherapy of Cancer. 2018, vol. 6, no. 60, p. 3
Abstract In a recent publication in Nature Communications the group of Dr. Dmitry Gabrilovich takes us one step closer to understanding why lipid accumulation impairs the function of tumour-associated dendritic cells (DCs). In this study, the authors present two surprising and significant findings. First, they show that in mouse DCs oxidized lipids function as a sink that traps the heat shock chaperone HSP70, a molecular target of emerging anti-cancer strategies. Secondly, they find that HSP70 in turn regulates the trafficking of peptide-loaded major histocompatibility complex class I (pMHC-I) molecules, a complex that triggers the proliferation of cancer-killing T cells. These observations are discussed briefly in the context of lipid droplet function and pMHC-I trafficking in tumour-associated DCs, as well as HSP70’s pleiotropic and incompletely understood roles - and what they mean for future cancer therapy designs.
Keywords Heat-shock proteinHspa1aHsp72mLipid bodiesAntigen presentationCross-presentation
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PMID: 29921314
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Research group Signaux intracellulaires (210)
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NUNES-HASLER, Paula. Oxidized lipids keep heat shock chaperones busy: new insights on the deficiencies of tumour-associated dendritic cells. In: Journal for ImmunoTherapy of Cancer, 2018, vol. 6, n° 60, p. 3. https://archive-ouverte.unige.ch/unige:107795

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Deposited on : 2018-09-14

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