Canonical IRE1 function needed to sustain vigorous natural killer cell proliferation during viral infection
- Author
- Jessica Vetters (UGent) , Mary van Helden (UGent) , Clint De Nolf (UGent) , Sofie Rennen (UGent) , Eva Cloots (UGent) , Evelien Van De Velde (UGent) , Farzaneh Fayazpour (UGent) , Justine Van Moorleghem (UGent) , Manon Vanheerswynghels (UGent) , Karl Vergote (UGent) , Louis Boon, Eric Vivier, Bart Lambrecht (UGent) and Sophie Janssens (UGent)
- Organization
- Project
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- Regulation of goblet cell homeostasis by the AGR2-IRE1b axis
- A novel role for the IRE1/XBP1 branch in dendritic cells: a signaling cascade matures
- The role of the IRE-1/XBP-1 axis in NK cell mediated anti-tumor immunology
- Refining cancer cell death and danger signals for the improvement of immunotherapy
- Abstract
- The unfolded protein response (UPR) aims to restore ER homeostasis under conditions of high protein folding load, a function primarily serving secretory cells. Additional, non-canonical UPR functions have recently been unraveled in immune cells. We addressed the function of the inositol-requiring enzyme 1 (IRE1) signaling branch of the UPR in NK cells in homeostasis and microbial challenge. Cell-intrinsic compound deficiency of IRE1 and its downstream transcription factor XBP1 in NKp46+ NK cells, did not affect basal NK cell homeostasis, or overall outcome of viral MCMV infection. However, mixed bone marrow chimeras revealed a competitive advantage in the proliferation of IRE1-sufficient Ly49H+NK cells after viral infection. CITE-Seq analysis confirmed strong induction of IRE1 early upon infection, concomitant with the activation of a canonical UPR signature. Therefore, we conclude that IRE1/XBP1 activation is required during vigorous NK cell proliferation early upon viral infection, as part of a canonical UPR response.
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-01HKCGKR2Z6V2480G7QAPK5SPC
- MLA
- Vetters, Jessica, et al. “Canonical IRE1 Function Needed to Sustain Vigorous Natural Killer Cell Proliferation during Viral Infection.” ISCIENCE, vol. 26, no. 12, 2023, doi:10.1016/j.isci.2023.108570.
- APA
- Vetters, J., van Helden, M., De Nolf, C., Rennen, S., Cloots, E., Van De Velde, E., … Janssens, S. (2023). Canonical IRE1 function needed to sustain vigorous natural killer cell proliferation during viral infection. ISCIENCE, 26(12). https://doi.org/10.1016/j.isci.2023.108570
- Chicago author-date
- Vetters, Jessica, Mary van Helden, Clint De Nolf, Sofie Rennen, Eva Cloots, Evelien Van De Velde, Farzaneh Fayazpour, et al. 2023. “Canonical IRE1 Function Needed to Sustain Vigorous Natural Killer Cell Proliferation during Viral Infection.” ISCIENCE 26 (12). https://doi.org/10.1016/j.isci.2023.108570.
- Chicago author-date (all authors)
- Vetters, Jessica, Mary van Helden, Clint De Nolf, Sofie Rennen, Eva Cloots, Evelien Van De Velde, Farzaneh Fayazpour, Justine Van Moorleghem, Manon Vanheerswynghels, Karl Vergote, Louis Boon, Eric Vivier, Bart Lambrecht, and Sophie Janssens. 2023. “Canonical IRE1 Function Needed to Sustain Vigorous Natural Killer Cell Proliferation during Viral Infection.” ISCIENCE 26 (12). doi:10.1016/j.isci.2023.108570.
- Vancouver
- 1.Vetters J, van Helden M, De Nolf C, Rennen S, Cloots E, Van De Velde E, et al. Canonical IRE1 function needed to sustain vigorous natural killer cell proliferation during viral infection. ISCIENCE. 2023;26(12).
- IEEE
- [1]J. Vetters et al., “Canonical IRE1 function needed to sustain vigorous natural killer cell proliferation during viral infection,” ISCIENCE, vol. 26, no. 12, 2023.
@article{01HKCGKR2Z6V2480G7QAPK5SPC,
abstract = {{The unfolded protein response (UPR) aims to restore ER homeostasis under conditions of high protein folding load, a function primarily serving secretory cells. Additional, non-canonical UPR functions have recently been unraveled in immune cells. We addressed the function of the inositol-requiring enzyme 1 (IRE1) signaling branch of the UPR in NK cells in homeostasis and microbial challenge. Cell-intrinsic compound deficiency of IRE1 and its downstream transcription factor XBP1 in NKp46+ NK cells, did not affect basal NK cell homeostasis, or overall outcome of viral MCMV infection. However, mixed bone marrow chimeras revealed a competitive advantage in the proliferation of IRE1-sufficient Ly49H+NK cells after viral infection. CITE-Seq analysis confirmed strong induction of IRE1 early upon infection, concomitant with the activation of a canonical UPR signature. Therefore, we conclude that IRE1/XBP1 activation is required during vigorous NK cell proliferation early upon viral infection, as part of a canonical UPR response.}},
articleno = {{108570}},
author = {{Vetters, Jessica and van Helden, Mary and De Nolf, Clint and Rennen, Sofie and Cloots, Eva and Van De Velde, Evelien and Fayazpour, Farzaneh and Van Moorleghem, Justine and Vanheerswynghels, Manon and Vergote, Karl and Boon, Louis and Vivier, Eric and Lambrecht, Bart and Janssens, Sophie}},
issn = {{2589-0042}},
journal = {{ISCIENCE}},
language = {{eng}},
number = {{12}},
pages = {{26}},
title = {{Canonical IRE1 function needed to sustain vigorous natural killer cell proliferation during viral infection}},
url = {{http://doi.org/10.1016/j.isci.2023.108570}},
volume = {{26}},
year = {{2023}},
}
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