The Role of SATB1 and the Treg/Th17 Cell Balance in Neuromyelitis Optica Spectrum Disorders
Objective:
This study aims to investigate changes in special AT-rich sequence-binding protein 1 (SATB1) and the balance between regulatory T cells (Treg) and T helper 17 cells (Th17) in neuromyelitis optica spectrum disorder (NMOSD).
Background:
The balance of Treg and Th17 cells is crucial for maintaining immune tolerance. SATB1 is associated with the function of Treg and Th17 cells. However, the role of SATB1 and Treg/Th17 cells in the pathogenesis of NMOSD remains to be elucidated.
Design/Methods:
This study included 40 patients with NMOSD, comprising 20 in the acute phase and 20 in the remission phase, with 20 healthy controls. We measured the mRNA expression of SATB1, FOXP3, and RORγt in CD4+ T cells, and quantified the proportions of Treg and Th17 cells in peripheral blood. Expanded Disability Status Scale (EDSS) scores, annual relapse rate (ARR), and the number of T2 lesions on MRI scans,were recorded and analyzed.
Results:
In NMOSD patients, SATB1 mRNA, RORγt mRNA, and Th17 cells were increased during the acute phase and elevated in remission compared to healthy controls. Conversely, FOXP3 mRNA and Treg cells were downregulated, more significantly in acute phase.A negative correlation was found between SATB1 and FOXP3 mRNA acutely (r = -0.92, P < 0.001), but not in remission (r = -0.44, P = 0.05).In both disease phases, SATB1 expression was positively correlated with RORγt mRNA (r=0.91, P<0.001; r=0.59, P<0.05) and Th17 cells (r=0.92, r=0.88, both P<0.0001), but negatively correlated with Treg cells (all r=-0.71; P<0.05).SATB1 mRNA levels positively correlated with clinical measures (EDSS: r=0.51/0.40; ARR: r=0.68/0.59; all P<0.05) but not with T2FLAIR lesions (r=0.14/0.04, P>0.05) in both acute and remission phases.
Conclusions:
SATB1 and Treg/Th17 correlate with clinical activity of NMOSD. SATB1 may act as a bridge in regulating the immune balance between Treg and Th17 cells, thereby influencing the progression of NMOSD.
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