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Innate lymphoid cells exhibited IL-17-expressing phenotype in active tuberculosis disease

Authors :
Yang Zheng
Wenjia Qiu
Xuanqi Liu
Xiangyang Li
Wei Xu
Yan Mou
Xiaoli Chen
Yunhuan Liu
Huili Zhu
Haiyan Ge
L. Pan
Wei-ping Jiang
Source :
BMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-11 (2021), BMC Pulmonary Medicine
Publication Year :
2021
Publisher :
BMC, 2021.

Abstract

Background Innate lymphoid cells (ILCs), as an important group of innate immunity, could respond rapidly to Mycobacterium tuberculosis (Mtb) infection. In this research, we studied the phenotypic changes of circulatory ILCs in active tuberculosis (TB) disease. Methods We recruited 40 patients with active Mtb infection (TB group) and 41 healthy subjects (NC group), and collected their clinical information and peripheral blood. Circulating ILCs, ILC subsets, dendritic cells (DCs), macrophages, and the production of cytokines in ILCs were tested by flow cytometry (FCM). Enzyme-linked immunosorbent assay (ELISA) was used to detect plasma IL-23. Results Compared with healthy control, total ILCs (0.73% vs. 0.42%, P = 0.0019), ILC1 (0.55% vs. 0.31%, P = 0.0024) and CD117+ ILC2 (0.02% vs. 0.01%, P = 0.0267) were upregulated in TB group. The total IL-17+ lymphocytes were elevated (3.83% vs. 1.76%, P = 0.0006) while the IL-22+ lymphocytes remained unchanged. Within ILC subsets, ILC3, CD117+ ILC2 and ILC1 in TB group all expressed increased IL-17 (15.15% vs. 4.55%, 19.01% vs. 4.57%, 8.79% vs. 3.87%, P P = 0.0557). Plasma IL-23 in TB group was positively correlated to IL-17+ ILC3 (r = 0.4435, P = 0.0141), IL-17+CD117+ ILC2 (r = 0.5385, P = 0.0021) and IL-17+ ILC1(r = 0.3719, P = 0.0430). TB group also had elevated DCs (9.35% vs. 6.49%, P + ILCs was related to severer inflammatory status and poorer clinical condition. Conclusions In active TB disease, circulatory ILCs were upregulated and exhibited IL-17-expressing phenotype. This may expand the understanding of immune reaction to Mtb infection.

Details

Language :
English
ISSN :
14712466
Volume :
21
Issue :
1
Database :
OpenAIRE
Journal :
BMC Pulmonary Medicine
Accession number :
edsair.doi.dedup.....d344e157fc6551c7a3cd84b8e650c70a