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

Sci Rep

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

Published: July 2020

MOG-antibody associated disease (MOG-AAD) is a recently recognized demyelinating disorder predominantly affecting children but also occurs in adults, with a relapsing course in approximately 50% of patients. We evaluated peripheral blood mononuclear cells from MOG-AAD patients by flow cytometry and found a strong antigen specific central memory cell (CMC) response with increased Th1 and Th17 cells at the time of a relapse. Transcriptomic analysis of CMCs by three independent sequencing platforms revealed TNFAIP3 as a relapse biomarker, whose expression was down regulated at a relapse compared to remission in MOG-AAD patients. Serum in an additional cohort of patients showed decreased TNFAIP3 levels at relapse compared to remission state in MOG-AAD patients. Our studies suggest that alterations in TNFAIP3 levels are associated with relapses in MOG-AAD patients, which may have clinical utility as a disease course biomarker and therapeutic target.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7381621PMC
http://dx.doi.org/10.1038/s41598-020-69182-wDOI Listing

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

Sci Rep

July 2020

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

MOG-antibody associated disease (MOG-AAD) is a recently recognized demyelinating disorder predominantly affecting children but also occurs in adults, with a relapsing course in approximately 50% of patients. We evaluated peripheral blood mononuclear cells from MOG-AAD patients by flow cytometry and found a strong antigen specific central memory cell (CMC) response with increased Th1 and Th17 cells at the time of a relapse. Transcriptomic analysis of CMCs by three independent sequencing platforms revealed TNFAIP3 as a relapse biomarker, whose expression was down regulated at a relapse compared to remission in MOG-AAD patients.

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