Identification of TNFAIP3 as relapse biomarker and potential therapeutic target for MOG antibody associated diseases

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Shrishti Saxena1, Hrishikesh Lokhande1, Grace Gombolay1,2,3

  • 1Ann Romney Center for Neurologic Disease, Brigham and Women's Hospital, Harvard Medical School, 60 Fenwood Road, Office 9002K, Boston, MA, 02115-6128, USA.

Scientific Reports
|July 26, 2020
PubMed

Insights

MOG-antibody associated disease (MOG-AAD) involves relapses. Researchers found TNFAIP3 levels decrease during MOG-AAD relapses, suggesting its potential as a biomarker.

Area of Science:

  • Neuroimmunology
  • Molecular Biology

Background:

  • MOG-antibody associated disease (MOG-AAD) is a demyelinating disorder with relapsing courses.
  • Understanding MOG-AAD relapse mechanisms is crucial for patient management.

Purpose of the Study:

  • To investigate immune cell responses during MOG-AAD relapses.
  • To identify biomarkers associated with MOG-AAD disease activity.

Main Methods:

  • Flow cytometry analysis of peripheral blood mononuclear cells (PBMCs) from MOG-AAD patients.
  • Transcriptomic analysis of central memory cells (CMCs) using three sequencing platforms.
  • Quantification of TNFAIP3 levels in patient serum samples.

Main Results:

  • Increased antigen-specific central memory cell (CMC) response, including Th1 and Th17 cells, observed during MOG-AAD relapses.
  • Downregulation of TNFAIP3 expression in CMCs during relapse compared to remission.
  • Decreased serum TNFAIP3 levels in MOG-AAD patients during relapse versus remission.

Conclusions:

  • Alterations in TNFAIP3 levels are linked to MOG-AAD relapses.
  • TNFAIP3 may serve as a valuable biomarker for monitoring MOG-AAD disease course.
  • TNFAIP3 represents a potential therapeutic target for MOG-AAD.

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