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

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

  • Nunes-Hasler P Department of Cell Physiology and Metabolism, University of Geneva, Faculty of Medicine, Rue Michel-Servet 1, 1211, Geneva, Switzerland. Paula.Nunes@unige.ch.
  • 2018-06-21
Published in:
  • Journal for immunotherapy of cancer. - 2018
Antigen presentation
Cross-presentation
Heat-shock protein
Hsp72m
Hspa1a
Lipid bodies
Animals
Dendritic Cells
HSP70 Heat-Shock Proteins
Heat-Shock Response
Humans
Lipids
Mice
Neoplasms
English 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.
Language
  • English
Open access status
gold
Identifiers
Persistent URL
https://sonar.ch/global/documents/46613
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