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NDRG1 is induced by antigen-receptor signaling but dispensable for B and T cell self-tolerance

Abstract:
Peripheral tolerance prevents the initiation of damaging immune responses by autoreactive lymphocytes. While tolerogenic mechanisms are tightly regulated by antigen-dependent and independent signals, downstream pathways are incompletely understood. N-myc downstream-regulated gene 1 (NDRG1), an anti-cancer therapeutic target, has previously been implicated as a CD4<sup>+</sup> T cell clonal anergy factor. By RNA-sequencing, we identified Ndrg1 as the third most upregulated gene in anergic, compared to naïve follicular, B cells. Ndrg1 is upregulated by B cell receptor activation (signal one) and suppressed by co-stimulation (signal two), suggesting that NDRG1 may be important in B cell tolerance. However, though Ndrg1<sup>-/-</sup> mice have a neurological defect mimicking NDRG1-associated Charcot-Marie-Tooth (CMT4d) disease, primary and secondary immune responses were normal. We find that B cell tolerance is maintained, and NDRG1 does not play a role in downstream responses during re-stimulation of in vivo antigen-experienced CD4<sup>+</sup> T cells, demonstrating that NDGR1 is functionally redundant for lymphocyte anergy.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s42003-022-04118-w

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Role:
Author
ORCID:
0000-0002-9157-045X
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Role:
Author
ORCID:
0000-0003-4528-0651
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Role:
Author
ORCID:
0000-0002-8543-6801
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Role:
Author


Publisher:
Springer Nature
Journal:
Communications Biology More from this journal
Volume:
5
Issue:
1
Article number:
1216
Place of publication:
England
Publication date:
2022-11-10
Acceptance date:
2022-10-17
DOI:
EISSN:
2399-3642
Pmid:
36357486


Language:
English
Keywords:
Pubs id:
1304570
Local pid:
pubs:1304570
Deposit date:
2024-05-13

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