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Updated: Jan 29, 2026
Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
Published on: August 21, 2017
Foxp3+ regulatory T cells expression in neuromyelitis optica spectrum disorders
Livnat Brill1, Iris Lavon2, Adi Vaknin-Dembinsky1
1Department of Neurology and the Multiple Sclerosis Center, the Agnes-Ginges Center for Neurogenetics, Hadassah- Medical Center, Hebrew University, Ein Karem, P.O.B. 12000, Jerusalem 91120, Israel.
Background:
Alterations in the frequency or function of regulatory T cells (Tregs), which play a critical role in the maintenance of peripheral immune tolerance, are known to be involved in the pathogenesis of several autoimmune diseases. Neuromyelitis optica spectrum disorders (NMOSD) are autoimmune inflammatory diseases of the central nervous system (CNS), of which the etiology and mechanisms underlying its development are not completely understood. Although there is increasing evidence for the involvement of effector T cells in NMOSD, no data are available regarding the role of Tregs in its pathogenesis.
Aim:
The aim of this study was to investigate the mRNA expression level of regulatory T cell genes in NMOSD.
Methods:
We used gene expression array and RT-PCR analysis to study Treg cell genes in NMOSD RESULTS: A distinctive Treg gene signature in the peripheral blood of NMOSD patients is described, as well as significantly decreased FoxP3 mRNA expression in the peripheral blood mononuclear cells (PBMCs) of the patients vs that in the healthy controls (HCs) (NMOSD,1.8RQ vs HC, 6.8RQ, p = 0.01).
Conclusions:
The present study shows downregulation at the mRNA expression level of a Treg key transcription factor FoxP3, in NMOSD. Exploration of Tregs function and interconnections in the peripheral immune system should advance our understanding of NMOSD pathogenesis.
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