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

Rose Hodgson1,2, Xijin Xu1,2, Consuelo Anzilotti1,2

  • 1MRC Human Immunology Unit, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Communications Biology
|November 10, 2022
PubMed

Insights

N-myc downstream-regulated gene 1 (NDRG1) is not essential for lymphocyte anergy in mice. Despite its upregulation in anergic B cells, NDRG1 does not play a critical role in maintaining peripheral tolerance.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Peripheral tolerance prevents autoimmune diseases by controlling autoreactive lymphocytes.
  • Downstream molecular pathways regulating tolerance are not fully understood.
  • N-myc downstream-regulated gene 1 (NDRG1) was previously suggested to induce T cell anergy.

Purpose of the Study:

  • To investigate the role of NDRG1 in B cell tolerance and lymphocyte anergy.
  • To determine if NDRG1 is essential for maintaining peripheral immune tolerance.

Main Methods:

  • RNA sequencing of anergic versus naïve B cells.
  • Analysis of immune responses in Ndrg1 knockout mice.
  • Assessment of T cell re-stimulation in vivo.

Main Results:

  • Ndrg1 was significantly upregulated in anergic B cells compared to naïve B cells.
  • Ndrg1 deficiency in mice did not impair primary or secondary immune responses.
  • NDRG1 was found to be functionally redundant for lymphocyte anergy.

Conclusions:

  • NDRG1 is not a critical factor for establishing or maintaining B cell tolerance.
  • The role of NDRG1 in immune regulation appears to be functionally redundant.
  • Further research is needed to fully elucidate the molecular mechanisms of peripheral tolerance.

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