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CD38: Modulating Histone Methyltransferase EZH2 Activity in SLE.

Paramita Chakraborty1, Shikhar Mehrotra1

  • 1Department of Surgery, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.

Trends in Immunology
|February 17, 2020
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Summary

Immunosuppression for SLE patients risks infection by impairing T cells. Targeting the CD38/NAD/Sirtuin1/EZH2 pathway may restore CD8+ T cell function and reduce infection incidence.

Keywords:
CD38EZH2SLET cellsmethylation

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • Systemic Lupus Erythematosus (SLE) requires immunosuppression, increasing infection risk.
  • Cytolytic CD8+ T cells are crucial for controlling infections but can be impaired in SLE patients.

Purpose of the Study:

  • To investigate the CD38/NAD/Sirtuin1/EZH2 pathway's role in regulating CD8+ T cell function in SLE.
  • To identify potential therapeutic targets to mitigate infection susceptibility in SLE patients.

Main Methods:

  • Analysis of the CD38/NAD/Sirtuin1/EZH2 molecular axis.
  • Assessment of CD8+ T cell function in the context of SLE.

Main Results:

  • The CD38/NAD/Sirtuin1/EZH2 pathway was shown to reduce the function of cytolytic CD8+ T cells.
  • This pathway represents a potential target for therapeutic intervention.

Conclusions:

  • The CD38/NAD/Sirtuin1/EZH2 axis negatively impacts CD8+ T cell immunity in SLE.
  • Targeting this pathway could enhance immune responses and reduce infection rates in SLE patients.