IL-33 mediates the immune regulation mechanism of brucellosis by regulating Treg cell function
10.3969/j.issn.1673-4130.2024.18.002
- VernacularTitle:IL-33介导Treg细胞功能参与布鲁氏菌病免疫调节机制研究
- Author:
Zhiwei LI
1
;
Zaokeran·Aliken
;
Lingling WANG
;
Jintong JIA
;
Shuling LI
;
Xiaoyu ZHU
;
Qian WANG
;
Peipei LU
;
Changmin WANG
Author Information
1. 新疆维吾尔自治区人民医院临床检验中心,新疆乌鲁木齐 830001
- Keywords:
brucellosis;
interleukin-33;
regulatory T cells;
immune mechanism
- From:
International Journal of Laboratory Medicine
2024;45(18):2184-2188,2196
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the characteristics of changes in interleukin(IL)-33 and regulatory T(Treg)cells in brucellosis,to verify the regulatory effect of IL-33 on Treg cells,so as to clarify the immune mechanism of IL-33 on Treg cells in brucellosis.Methods The peripheral blood of 39 patients with brucellosis treated in the People's Hospital of Xinjiang Uygur Autonomous Region from January to December 2021(the brucellosis group)and 42 healthy controls(the healthy control group)who underwent physical examination during the same period were collected.The serum IL-33 level was detected by AimPlex kit,and the proportion of Treg cells was detected by flow cytometry.Peripheral blood mononuclear cell(PBMC)was extracted and cultured in vitro to observe the proportion and mRNA expression levels of forkhead box protein P3(Foxp3)after stimulation and blocking of IL-33.Results Compared with the healthy control group,the level of IL-33 and the proportion of Treg cells in brucellosis group were significantly increased,with statistical significance(P＜0.05).In vitro tests showed that the Foxp3 proportion and mRNA expression level of PBMC in the two groups were significantly increased after IL-33 stimulation,and significantly decreased after IL-33 blocking,with statistical significance(P＜0.001).Conclusion IL-33 and Treg cells increased significantly in brucellosis patients,and IL-33 promoted the immune function of Treg cells.Blocking IL-33 is expected to be a potential target for immunotherapy of brucellosis.
