Myeloid-derived suppressor cells as biomarkers of the effectiveness of therapy with new biological agents in axial spondyloarthritis

نویسندگان

چکیده

Innate immune cells, including myeloid cells — derived suppressor (MDSCs) are supposed to play an important role in the pathogenesis of axial spondyloarthritis (AxSp). Myeloid represent a heterogeneous population immature capable suppressing innate and adaptive responses with most pronounced activity against T cells. Biological disease-modifying antirheumatic drugs (bDMARDs) can reduce clinical laboratory disease activity, but their effectiveness varies widely different patients AxSp. The present study is aimed at studying MDSCs subpopulations suppressive function depending on response bDMARD therapy included AxSp duration 16.5 years (median); HLA-B27 (+) status was detected 79% cases. All received bDMARDs least past 12 weeks, TNF inhibitors (etanercept, certolizumab pegol, adalimumab, or golimumab) IL-17 (secukinumab, ixekizumab, netakimab). Percentage granulocytic (G-MDSCs, Lin - HLA-DR-CD33 + CD66b ), monocytic (M-MDSCs, HLA-DR low/- CD14 early stage differentiation (E-MDSCs, CD33 as well intracellular expression arginase-1 assessed by flow cytometry. Frequency circulating MDSC stable (responders) did not differ significantly compared healthy donors. Patients responding showed increased relative absolute number E-MDSCs donors (p U = 0.01 p 0.02, respectively) responders 0.03 0.07, respectively). Increased percentage positively correlated ESR (R s 0.821; 0.023), CRP 0.714; 0.07) ASDAS 0.829; 0.042) non-responder group. Responder exhibited no correlation between MDSCs. potential analyzed molecule which involved inhibition cell response. were characterized 0.02). Non-responders demonstrate significant changes Arg-1 expression, however, arginase-1-expressing G-MDSCs indexes 0.857; 0.014) BASDAI 0.785; 0.036). Thus, may serve biomarkers therapy, act candidate predictors

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ژورنال

عنوان ژورنال: ??????????? ???????????

سال: 2023

ISSN: ['2409-5788']

DOI: https://doi.org/10.15789/1563-0625-mds-2696