Abstract：
Autoreactive CD4+ helper T cells are implicated in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD). Both PD-1+CXCR5+CD4+ T follicular helper (Tfh) cells and PD-1+CXCR5-CD4+ T peripheral helper (Tph) cells can contribute to B-cell immune responses and the production of antibodies. Here we show the effect of B-cell depletion with rituximab on the homeostasis of Tfh cells, Tph cells and their subsets in patients with NMOSD. After rituximab treatment, total Tph cells, total Tfh cells, Tph17 cells, Tph17.1 cells, Tph1 cells, and Tfh1 cells tended to decrease at month 1, but gradually increased at month 6 and restored at month 12. Besides, Tph17.1 cells and Tfh17.1 cells were correlated with the proportion of CD19- antibody-secreting cells. Our data suggest that rituximab induced a fluctuation of proinflammatory Tph and Tfh subsets within one year after initiation of the treatment.
摘要：
自身反应性CD4+辅助性T细胞参与视神经脊髓炎谱系障碍(NMOSD)的发病机理。PD-1+CXCR5+CD4+T滤泡辅助(Tfh)细胞和PD-1+CXCR5-CD4+T外周辅助(Tph)细胞均可有助于B细胞免疫应答和抗体的产生。在这里，我们显示了利妥昔单抗对Tfh细胞稳态的B细胞耗竭的影响，NMOSD患者的Tph细胞及其亚群。利妥昔单抗治疗后,Tph细胞总数,Tfh细胞总数,Tph17细胞,Tph17.1细胞，Tph1细胞，Tfh1细胞在第1个月时呈减少趋势，但在第6个月时逐渐增加，并在第12个月时恢复。此外,Tph17.1细胞和Tfh17.1细胞与CD19抗体分泌细胞的比例相关。我们的数据表明，利妥昔单抗在治疗开始后一年内引起促炎Tph和Tfh亚群的波动。
