The Q for immune evasion in HCC: ER stress in myeloid cells

Figure 1 A glutamine metabolism-ER stress-immune evasion axis in HCC.In HCC, metabolic competition with tumour cells leads to glutamine/Q shortage in myeloid cells.Q shortage induces ER stress in myeloid cells and increases the expression of the vitamin B 3 receptor GPR109A.GPR109A activation results in immunosuppressive polarisation and additional recruitment of myeloid cells.Subsequently, antitumour CD8+ T-cell immunity is impaired.ER, endoplasmic reticulum; HCC, hepatocellular carcinoma.

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Journal
Gut
Published
2024-08-29
DOI
https://doi.org/10.1136/gutjnl-2024-333249
Primary Topic
Endoplasmic Reticulum Stress and Disease
Type
article
Field-Weighted Citation Impact
0.00

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article

The Q for immune evasion in HCC: ER stress in myeloid cells

Charlotte Rennert, Maike Hofmann
Gut
Endoplasmic Reticulum Stress and Disease
article

The Q for immune evasion in HCC: ER stress in myeloid cells

Charlotte Rennert, Maike Hofmann
article en

Abstract

Figure 1 A glutamine metabolism-ER stress-immune evasion axis in HCC.In HCC, metabolic competition with tumour cells leads to glutamine/Q shortage in myeloid cells.Q shortage induces ER stress in myeloid cells and increases the expression of the vitamin B 3 receptor GPR109A.GPR109A activation results in immunosuppressive polarisation and additional recruitment of myeloid cells.Subsequently, antitumour CD8+ T-cell immunity is impaired.ER, endoplasmic reticulum; HCC, hepatocellular carcinoma.

GutVol. 74(2)
University of Freiburg (DE), University Medical Center Freiburg (DE)
Deutsche Forschungsgemeinschaft, Else Kröner-Fresenius-Stiftung
Zero hunger
Openalex Percentile: Top 85%
Endoplasmic Reticulum Stress and Disease
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