Luya Cheng1, Chanjuan Liu2, Feng Li3, Boting Wu4, Zhihui Min5, Pu Chen6, Yanxia Zhan7, Yang Ke8, Fanli Hua9, Ling Yuan10, Lihua Sun11, Hao Chen12, Lili Ji13, Yunfeng Cheng14. 1. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: cheng.luya@zs-hospital.sh.cn. 2. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: 15111210015@fudan.edu.cn. 3. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China; Department of Hematology, Zhongshan Hospital Qingpu Branch, Fudan Universiy, Shanghai 201700, China. Electronic address: li.feng@zs-hospital.sh.cn. 4. Department of Transfusion Medicine, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: wu.boting@zs-hospital.sh.cn. 5. Institute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Department of Thoracic Surgery, Zhongshan Hospital Xuhui Branch, Fudan University, Shanghai 200031, China. Electronic address: min.zhihui@zs-hospital.sh.cn. 6. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: chen.pu@zs-hospital.sh.cn. 7. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: zhan.yanxia@zs-hospital.sh.cn. 8. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: ke.yang@zs-hospital.sh.cn. 9. Department of Hematology, Zhongshan Hospital Qingpu Branch, Fudan Universiy, Shanghai 201700, China. Electronic address: hua_fanli@fudan.edu.cn. 10. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: yuan.ling@zs-hospital.sh.cn. 11. Department of Hematology, Zhongshan Hospital Qingpu Branch, Fudan Universiy, Shanghai 201700, China. 12. Department of Thoracic Surgery, Zhongshan Hospital Xuhui Branch, Fudan University, Shanghai 200031, China. Electronic address: h.chen@fudan.edu.cn. 13. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China. Electronic address: ji.lili@zs-hospital.sh.cn. 14. Department of Hematology, Zhongshan Hospital Fudan University, Shanghai 200032, China; Department of Hematology, Zhongshan Hospital Qingpu Branch, Fudan Universiy, Shanghai 201700, China; Institute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Center for Tumor Diagnosis & Therapy, Jinshan Hospital, Fudan University, Shanghai, 201500, China. Electronic address: yfcheng@fudan.edu.cn.
Abstract
BACKGROUND: Primary immune thrombocytopenia (ITP) is an autoimmune heterogeneous disorder of which Treg cells are numerically or functionally deficient. It is known that human FoxP3+CD4+ T cells were composed of 3 phenotypically and functionally distinct subpopulations (resting Treg, rTreg; activated Treg, aTreg; and non-suppressive Treg, n-sTreg). The current study was aimed to determine whether these Treg subtypes are altered in ITP patients and the related potential clinical applications. METHOD: Normal control volunteers and newly diagnosed ITP patients were enrolled in the study. The percentage of Treg cells' subtypes in peripheral blood was examined by flow cytometry before and after the glucocorticoid treatment. The IL-10 production by Treg subtypes was also examined. RESULTS: Treg cell subtypes of aTreg increased, rTreg decreased, and n-s Treg increased in newly diagnosed ITP patients' peripheral blood. The IL-10 production by respective Treg subtype didn't change after the treatment, and aTreg cells had the highest IL-10 yield. Patients who gained remission during follow-up had a higher aTreg cells' percentage than those who did not at the disease diagnosis. CONCLUSION: Tregs cell subtypes percentage was altered when ITP occurred. The increased aTreg cells at disease diagnosis might predict a better glucocorticoid treatment efficacy.
BACKGROUND:Primary immune thrombocytopenia (ITP) is an autoimmune heterogeneous disorder of which Treg cells are numerically or functionally deficient. It is known that humanFoxP3+CD4+ T cells were composed of 3 phenotypically and functionally distinct subpopulations (resting Treg, rTreg; activated Treg, aTreg; and non-suppressive Treg, n-sTreg). The current study was aimed to determine whether these Treg subtypes are altered in ITP patients and the related potential clinical applications. METHOD: Normal control volunteers and newly diagnosed ITP patients were enrolled in the study. The percentage of Treg cells' subtypes in peripheral blood was examined by flow cytometry before and after the glucocorticoid treatment. The IL-10 production by Treg subtypes was also examined. RESULTS: Treg cell subtypes of aTreg increased, rTreg decreased, and n-s Treg increased in newly diagnosed ITP patients' peripheral blood. The IL-10 production by respective Treg subtype didn't change after the treatment, and aTreg cells had the highest IL-10 yield. Patients who gained remission during follow-up had a higher aTreg cells' percentage than those who did not at the disease diagnosis. CONCLUSION: Tregs cell subtypes percentage was altered when ITP occurred. The increased aTreg cells at disease diagnosis might predict a better glucocorticoid treatment efficacy.