美罗华
CD19
视神经脊髓炎
免疫学
CXCR5型
白细胞介素21
抗体
细胞毒性T细胞
CD40
免疫系统
B细胞
T细胞
医学
化学
生发中心
体外
生物化学
作者
Zhenning Huang,Ye Liu,Xueting An,Chen Zhang,Tianxiang Zhang,Huining Li,Bin Feng,Yanyan Li,Chao Zhang
标识
DOI:10.1016/j.jneuroim.2023.578167
摘要
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.
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