Abstract
Objective. This study aimed to examine the potential role of memory T follicular helper (Tfh) cells in patients with neuromyelitis optica/neuromyelitis optica spectrum disorders (NMO/NMOSD). Methods. The percentages of different subsets of circulating memory Tfh cells in 25 NMO/NMOSD patients before and after treatment as well as in 17 healthy controls were examined by flow cytometry. The levels of IL-21 and AQP4 Ab in plasma and CSF were measured by ELISA. Results. The percentages and numbers of circulating memory Tfh cells, ICOS+, CCR7−, CCR7−ICOS+, CCR7+, CCR7+ICOS+ memory Tfh cells, and the levels of IL-21 in plasma and CSF were significantly increased in NMO/NMOSD patients. The percentages of CCR7− and CCR7−ICOS+ memory Tfh cells were positively correlated with ARR, plasma IL-21, and AQP4 Ab levels. The percentages of CCR7+ and CCR7+ICOS+ memory Tfh cells were positively correlated with CSF white blood cell counts, proteins, and IL-21 levels. Treatment with corticosteroids significantly reduced the numbers of CCR7−ICOS+ and CCR7+ICOS+ memory Tfh cells as well as plasma IL-21 levels in patients with partial remission. Conclusions. Our findings indicate that circulating memory Tfh cells may participate in the relapse and development of NMO/NMOSD and may serve as a new therapeutic target.
Highlights
After a primary response, most effector T cells undergo apoptosis, whereas a small proportion survive and become memory T cells [1]
We measured the percentages and numbers of different subsets of circulating memory T follicular helper (Tfh) cells (CD3+CD4+CXC-chemokine receptor 5 (CXCR5)+CD45RA− T cells) in Neuromyelitis optica (NMO)/NMO spectrum disorders (NMOSD) patients before and after treatment as well as in healthy controls (HCs) (Figure 1(a)). Both the percentages of memory Tfh cells and inducible costimulator (ICOS)+ memory Tfh cells among CD4+ T cells were significantly greater in NMO/NMOSD patients before treatment than those in the HC group (P = 0.001 and P = 0.0001, resp.; Figures 1(b) and 1(c))
We found that the percentages of CCR7− and CCR7−ICOS+ memory Tfh cells were positively correlated with the annual relapse rate (ARR; Figures 6(a) and 6(b)) and with the levels of plasma IL-21 in the NMO/NMOSD patients (Figures 6(c) and 6(d))
Summary
Most effector T cells undergo apoptosis, whereas a small proportion survive and become memory T cells [1]. Memory T cells induce a potent and quick secondary response upon antigen rechallenge and participate in the pathogenesis of recurrent autoimmune diseases [1, 2]. NMO spectrum disorders (NMOSD) are limited forms of NMO, including optic-spinal multiple sclerosis, relapsing isolated optic neuritis, recurrent transverse myelitis, and optic neuritis or myelitis in the context of certain autoimmune diseases [4]. It is generally accepted that NMO/NMOSD are complicated immunological disorders mainly involving humoral immunity [5, 6]. A recent study showed that memory Th17 cells are involved in the development and relapse of NMO, whereas intravenous methylprednisolone reduces memory Th17 proportions [2]. How memory T cell immunity regulates humoral immunity during relapse in NMO/NMOSD patients has not been clarified
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