Abstract：
The relapses and refractory disease are a challenge in the management of patients with Takayasu arteritis (TAK). We quantified pathogenic CD4 + memory T helper cells bearing surface markers CD161 and/or p-glycoprotein (MDR1) in patients with TAK. Peripheral blood mononuclear cells of 21 patients with TAK and 16 age-matched controls were stained with anti-CD3, anti-CD4, anti-CD45RA, anti-CD161 and anti-p-glycoprotein antibodies and subjected to flow cytometry by FACS ARIAIII. Eighteen patients underwent follow-up immunophenotyping. Intracellular staining for interleukin-17 and interferon-γ was performed for 18 patients and 11 controls. Surgical arterial biopsies of 6 TAK and 5 non-inflammatory controls were subjected to immunohistochemistry with anti-CD161 and anti-p-glycoprotein. At baseline the frequency of MDR1 + CD4 + and CD161 + MDR1 + CD4 + memory T cells was higher in TAK than controls (p = 0.002 and 0.01, respectively). After stimulation, the frequency of IFN-y + CD161 + cells was higher in TAK than controls (p = 0.028). Modal fluorescence intensity of CD161 + MDR1 + CD45RA - CD4 + cells was higher in active as compared with stable disease (p = 0.041). At 6 months, MDR1 + and CD161 + MDR1 + memory CD4 + T cells decreased significantly only in patients who had complete/partial response to treatment (p = 0.047 and 0.02, respectively). To conclude, MDR1 + and MDR1 + CD161 + CD4 + memory T-helper cells are increased in patients with TAK. These cells decreased only in patients with response to treatment during subsequent follow-up.
摘要：
复发和难治性疾病是治疗Takayasu动脉炎（TAK）患者的挑战。我们定量了TAK患者中带有表面标志物CD161和/或p-糖蛋白（MDR1）的致病性CD4记忆T辅助细胞。对21例TAK患者和16例年龄匹配的对照者外周血单个核细胞进行抗CD3、抗CD4、抗CD45RA染色,抗CD161和抗P-糖蛋白抗体，并通过FACSARIAIII进行流式细胞术。18例患者接受了随访免疫分型。对18例患者和11例对照进行了白细胞介素17和干扰素γ的细胞内染色。对6个TAK和5个非炎性对照的外科动脉活检进行抗CD161和抗P-糖蛋白的免疫组织化学。在基线时，TAK中MDR1CD4和CD161MDR1CD4记忆T细胞的频率高于对照组（分别为p=0.002和0.01）。刺激后,TAK中IFN-y+CD161+细胞的频率高于对照组(p=0.028)。与疾病稳定相比，CD161MDR1CD45RA-CD4细胞的模态荧光强度更高（p=0.041）。6个月时,MDR1和CD161MDR1记忆CD4T细胞仅在对治疗有完全/部分反应的患者中显着降低（分别为p=0.047和0.02）。最后，TAK患者MDR1+和MDR1+CD161+CD4+记忆T辅助细胞增加。这些细胞仅在随后的随访期间对治疗有反应的患者中减少。
