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Evaluating the diversity of circulating natural killer cells between active tuberculosis and latent tuberculosis infection
被引:7
|作者:
Zhou, Yu
[1
]
Lan, Haiping
[2
]
Shi, Hanlu
[3
]
Wu, Peihao
[4
]
Zhou, Yonglie
[1
]
机构:
[1] Hangzhou Med Coll, Affiliated Peoples Hosp, Zhejiang Prov Peoples Hosp, Lab Med Ctr,Dept Clin Lab, Hangzhou, Peoples R China
[2] Hangzhou Normal Univ, Affiliated Hosp, Dept TB, Hangzhou 310015, Zhejiang, Peoples R China
[3] Zhejiang Chinese Med Univ, Sch Med Technol & Informat Engn, Hangzhou 310053, Zhejiang, Peoples R China
[4] Zhejiang Univ, Womens Hosp, Sch Med, Dept Clin Lab, Hangzhou 310006, Zhejiang, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
Active tuberculosis;
Latent tuberculosis infection;
Natural killer cell;
KLRG1;
NKG2D;
NK-CELLS;
INDIVIDUALS;
SUBSETS;
PATHWAY;
D O I:
10.1016/j.tube.2022.102221
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Tuberculosis (TB) is a leading global public health problem; however, the mechanisms underlying the immunopathology of TB progression are not well understood. It is currently believed that Mycobacterium tuberculosis (Mtb) infection can modify natural killer (NK) cell phenotypic signatures. Hence, our study was designed to investigate the diversity of circulating NK cells in patients with different TB infection status. NK subsets, as well as their expression of activating and inhibitory receptors between active TB (ATB) and latent TB infection (LTBI) were evaluated. There were significant differences in NK cell phenotypes between ATB, LTBI and healthy controls. Notably, the proportion of KLRG1 in NK cells (P = 0.036), as well as in their subsets CD56DimCD16+ (P = 0.046) and CD27+ (P = 0.027) NK cells, increased significantly in LTBI group than in ATB group; while Mtb specific IFN-??+CD56BrightCD16Dim NK cells expressed higher KLRG1 in ATB than in LTBI (P = 0.027). However, the expression of activating receptor NKG2D in NK subsets showed no significant difference among the study groups. Our results suggest that different TB infection status are coupled with the diversity of NK cell compartments, and the expression of KLRG1 in NK cells may be a specific phenotype that modulates the progression of TB from latent to active.
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