Skip to main content
Log in

BCL-6 and EZH2 cooperate to epigenetically repress anti-inflammatory miR-142-3p/5p in lupus CD4+T cells

  • Comment
  • Published:
Cellular & Molecular Immunology Submit manuscript

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1

References

  1. Sawalha, A. H. Clinical immunology: a special issue on epigenetics. Clin. Immunol. 196, 1–2 (2018).

    Article  CAS  Google Scholar 

  2. Surace, A. E. A. & Hedrich, C. M. The role of epigenetics in autoimmune/inflammatory disease. Front. Immunol. 10, 1525 (2019).

    Article  CAS  Google Scholar 

  3. Ballestar, E. & Li, T. New insights into the epigenetics of inflammatory rheumatic diseases. Nat. Rev. Rheumatol. 13, 593–605 (2017).

    Article  CAS  Google Scholar 

  4. Weeding, E. & Sawalha, A. H. Deoxyribonucleic acid methylation in systemic lupus erythematosus: implications for future clinical practice. Front. Immunol. 9, 875 (2018).

    Article  Google Scholar 

  5. Hedrich, C. M. Epigenetics in SLE. Curr. Rheumatol. Rep. 19, 58 (2017).

    Article  Google Scholar 

  6. Coit, P. et al. Renal involvement in lupus is characterized by unique DNA methylation changes in naive CD4+ T cells. J. Autoimmun. 61, 29–35 (2015).

    Article  CAS  Google Scholar 

  7. Renauer, P. et al. DNA methylation patterns in naive CD4+ T cells identify epigenetic susceptibility loci for malar rash and discoid rash in systemic lupus erythematosus. Lupus Sci. Med. 2, e000101 (2015).

    Article  Google Scholar 

  8. Mok, A. et al. Genome-wide profiling identifies associations between lupus nephritis and differential methylation of genes regulating tissue hypoxia and type 1 interferon responses. Lupus Sci. Med. 3, e000183 (2016).

    Article  Google Scholar 

  9. Coit, P. et al. Ethnicity-specific epigenetic variation in naive CD4+ T cells and the susceptibility to autoimmunity. Epigenet. Chromatin 8, 49 (2015).

    Article  Google Scholar 

  10. Zhao, M. et al. IFI44L promoter methylation as a blood biomarker for systemic lupus erythematosus. Ann. Rheum. Dis. 75, 1998–2006 (2016).

    Article  CAS  Google Scholar 

  11. Coit, P. et al. Epigenetic reprogramming in naive CD4+ T cells favoring T cell activation and non-Th1 effector T cell immune response as an early event in lupus flares. Arthritis Rheumatol. 68, 2200–2209 (2016).

    Article  CAS  Google Scholar 

  12. Tsou, P. S., Coit, P., Kilian, N. C. & Sawalha, A. H. EZH2 modulates the DNA methylome and controls T cell adhesion through junctional adhesion molecule a in lupus patients. Arthritis Rheumatol. 70, 98–108 (2018).

    Article  CAS  Google Scholar 

  13. Rohraff D. M., et al. Inhibition of EZH2 ameliorates lupus-like disease in MRL/lpr mice. Arthritis Rheumatol. (2019). https://doi.org/10.1002/art.40931. [Epub ahead of print].

  14. Ding S., et al. BCL-6 suppresses miR-142-3p/5p expression by modulating histone methylation and acetylation of miR-142 promoter in SLE CD4+ T cells. Cell Mol. Immunol. 2019. https://doi.org/10.1038/s41423-019-0268-3. [Epub ahead of print].

  15. Ding, S. et al. Decreased microRNA-142-3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus. Arthritis Rheum. 64, 2953–2963 (2012).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Amr H. Sawalha.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Sawalha, A.H. BCL-6 and EZH2 cooperate to epigenetically repress anti-inflammatory miR-142-3p/5p in lupus CD4+T cells. Cell Mol Immunol 18, 504–505 (2021). https://doi.org/10.1038/s41423-019-0288-z

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s41423-019-0288-z

  • Springer Nature Limited

Navigation