Dan Xu1, Xiaoyu Liu2, Chengyang Lu3, Jing Luo1, Caihong Wang1, Chong Gao4, Jianfang Xie1, Xiaofeng Li5. 1. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China. 2. The Second Clinical Medical College of Shanxi Medical University, Taiyuan, China. 3. Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China. 4. Department of Pathology, Joint Program in Transfusion Medicine, Brigham and Women's Hospital/Children's Hospital Boston, Harvard Medical School, Boston, USA. 5. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China. lxf_9859@sxmu.edu.cn.
Abstract
OBJECTIVES: Little is known about the roles of peripheral immune cell subsets in synovitis, acne, pustulosis, hyperostosis and osteitis (SAPHO) syndrome. Up to now, just a few studies have focused on this issue. We aimed to analyse the distribution and phenotype of T cell subsets and natural killer (NK) cells in the peripheral blood of patients with SAPHO syndrome. METHODS: The proportion and absolute counts of circulating immune cells were assessed in 19 patients diagnosed as SAPHO syndrome and 19 healthy controls. CD4+T cell subsets were also analysed in 9 untreated SAPHO patients and 9 healthy volunteers by flow cytometry. RESULTS: The proportion and absolute counts of NK cells were significantly reduced in SAPHO patients in comparison with the controls (proportion, 10% vs. 18%, p<0.001; absolute counts, 231/μl vs. 307/μl, p=0.014). Conversely, the proportion and absolute counts of Th17 cells in untreated SAPHO patients were significantly higher than that in the healthy controls (proportion, 1.49% vs. 0.93%, p=0.004; absolute counts, 14.36/μl vs. 5.14/μl, p<0.001). Similarly, Th17/Th1 cells were significantly increased (proportion, 0.45% vs. 0.33%, p=0.024; absolute number, 5.47/μl vs. 1.98/μl, p<0.001), but there was no significant difference between the percentage and number of Treg cells in patients with SAPHO syndrome and healthy controls. Thus, the ratio of Th17/Treg was increased in SAPHO patients (0.68 vs. 0.17, p=0.004). CONCLUSIONS: Our data suggested that the immune inflammation in SAPHO patients may be related to the depletion of NK cells and the imbalance of Th17 and Treg cells. A reduction of peripheral NK cells may exacerbate the disease progression by not being inhibited Th17 cells.
OBJECTIVES: Little is known about the roles of peripheral immune cell subsets in synovitis, acne, pustulosis, hyperostosis and osteitis (SAPHO) syndrome. Up to now, just a few studies have focused on this issue. We aimed to analyse the distribution and phenotype of T cell subsets and natural killer (NK) cells in the peripheral blood of patients with SAPHO syndrome. METHODS: The proportion and absolute counts of circulating immune cells were assessed in 19 patients diagnosed as SAPHO syndrome and 19 healthy controls. CD4+T cell subsets were also analysed in 9 untreated SAPHO patients and 9 healthy volunteers by flow cytometry. RESULTS: The proportion and absolute counts of NK cells were significantly reduced in SAPHO patients in comparison with the controls (proportion, 10% vs. 18%, p<0.001; absolute counts, 231/μl vs. 307/μl, p=0.014). Conversely, the proportion and absolute counts of Th17 cells in untreated SAPHO patients were significantly higher than that in the healthy controls (proportion, 1.49% vs. 0.93%, p=0.004; absolute counts, 14.36/μl vs. 5.14/μl, p<0.001). Similarly, Th17/Th1 cells were significantly increased (proportion, 0.45% vs. 0.33%, p=0.024; absolute number, 5.47/μl vs. 1.98/μl, p<0.001), but there was no significant difference between the percentage and number of Treg cells in patients with SAPHO syndrome and healthy controls. Thus, the ratio of Th17/Treg was increased in SAPHO patients (0.68 vs. 0.17, p=0.004). CONCLUSIONS: Our data suggested that the immune inflammation in SAPHO patients may be related to the depletion of NK cells and the imbalance of Th17 and Treg cells. A reduction of peripheral NK cells may exacerbate the disease progression by not being inhibited Th17 cells.