Double-negative T cells are absolutely elevated in patients with antineutrophil cytoplasmic autoantibody-associated vasculitis.

CD3CD4CD8 [double-negative (DN)] T cells play vital roles in the pathogenesis of autoimmune disorders. In this study, we investigated the exact level of DN T cells in patients with antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV). Forty patients with active AAV and 19 healthy controls (HCs) were enrolled in this study. Peripheral mononuclear cells were characterised phenotypically via flow cytometry. The potential clinical value of DN T cells was then assessed by the receiver operating characteristic (ROC) curves. The percentage (p < 0.001) and absolute number (p = 0.028) of DN T cells were found to be significantly higher in patients with AAV than in HCs. Relative to HCs, a lower percentage of DN T cells from patients with AAV was of the CD62LCD45RO phenotype (p = 0.024), a higher percentage of these cells was of the CD62L-CD45RO- phenotype (p = 0.043). Patients with AAV had increased percentages of DN T cells expressing interferon (IFN)-γ (p = 0.032), interleukin (IL)-4 (p = 0.039) and IL-17 (p = 0.042). Furthermore, the percentages of IL-17-producing CD4 T cells and IFN-γ-producing CD8 T cells were significantly higher in patients with AAV than in HCs (p = 0.014, p = 0.008). Compared with the CD4 and CD8 T-cell subsets, DN T cells had the highest fractions of intracellular IL-17 in HCs and patients with AAV (both p < 0.001). In patients with AAV and renal damage, the percentage of DN T cells was expanded relative to that in patients without renal damage (p = 0.016). In addition, conventional methylprednisolone effectively reduced the percentage and overall number of DN T cells in patients with AAV (p = 0.028, p = 0.007). DN T cells represent a T-lymphocyte subset that produces inflammatory cytokines (IFN-γ, IL-4 and IL-17) and is absolutely elevated in patients with AAV. Additional investigations are required to determine their precise role in patients with AAV.