Research Papers: Immunology:
Re-balance of memory T cell subsets in peripheral blood from patients with CML after TKI treatment
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Danlin Yao1,2,*, Ling Xu1,2,*, Jiaxiong Tan1,2, Yikai Zhang1,2, Shuai Lu1, Mingde Li1,2, Sichun Lu1,2, Lijian Yang1, Shaohua Chen1, Jie Chen2, Jing Lai2, Yuhong Lu2, Xiuli Wu1,2, Xianfeng Zha3 and Yangqiu Li1,2
1 Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, School of Medicine, Jinan University, Guangzhou, China
2 Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, China
3 Department of Clinical Laboratory, First Affiliated Hospital, Jinan University, Guangzhou, China
* These authors have contributed equally to this work
Yangqiu Li, email:
Keywords: memory T cells, TSCM, CML, TKI, Immunology and Microbiology Section, Immune response, Immunity
Received: June 28, 2017 Accepted: August 27, 2017 Published: September 16, 2017
T cell immune surveillance is considered an important host protection process for inhibiting carcinogenesis. The full capacity of T cell immune surveillance is dependent on T cell homeostasis, particularly for central memory T (TCM) cells and stem cell memory T (TSCM) cells. In this study, distribution of T cell subsets in peripheral blood from 12 patients with chronic myeloid leukemia (CML) and 12 cases with CML in complete remission (CR) was analyzed using a multicolor flow cytometer, and 16 samples from healthy individuals (HIs) served as control. The proportion of CD8+ TSCM and CD4+ and CD8+ TCM cells were lower, while CD4+ effector memory T (TEM) cells and CD4+ and CD8+ terminal effector T (TEF) cells were higher in CML patients compared with HIs. Moreover, the proportion of CD8+CD28- T cells, which were found to have the immune suppressive function, increased in the naive T (TN) cell and TCM subsets in CML patients compared with HIs. Our study reveals that elimination of leukemia cells by treating with tyrosine kinase inhibitors (TKIs) restores the memory T cell distribution from a skewed pattern in CML patients who are under leukemia burden, indicating that leukemia-specific immune responses mediated by T cells might be induced and maintained in CML patients, however, these responsive T cells might gradually become exhausted due to the continued existence of leukemia cells and their environment; therefore, T cell activation using a different approach remains a key point for enhancing global T cell immunity in CML patients, even for those with CR status.
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