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Updated: May 19, 2026

Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
Published on: September 18, 2020
[The balance of Th1 and Th17 cells in tuberculous pleural effusion]
Rong-hui Du1, Tan-ze Cao, Zhan Lian
1Department of Internal Medicine, Wuhan Institute of Tuberculosis Prevention and Control, China.
Objective:
The aim of this study was to investigate the distributions and relevance of Th1 and Th17 cells (IL-17-producing CD(+)(4) T cell), and the differentiation of Th17 cells in tuberculous pleural effusion.
Methods:
The percentages of both Th1 and Th17 cells in tuberculous pleural effusion and peripheral blood from 30 patients [male/female 12/18, age 16 - 63 years (average 41.2 year)] with tuberculous pleurisy were determined by flow cytometry, and comparison was made using Student's t test. The regulations of different combinations of IFN-γ, IL-1β, IL-6 and IL-12 on differentiation of Th17 cells were explored. Comparisons of the data between different groups were performed using Kruskal-Wallis one-way analysis of variance on ranks.
Results:
Both Th1 [(39 ± 11)% vs (8 ± 3)%; t = 17.37, P < 0.05] and Th17 cells [(2.8 ± 0.9)% vs (0.7 ± 0.3)%; t = 14.78, P < 0.05] were significantly increased in tuberculous pleural effusion compared with peripheral blood. The proportions of Th17 cells were correlated positively with those of Th1 cells both in tuberculous pleural effusion and in peripheral blood (r = 0.61, 0.49, respectively; both P < 0.05). IL-1β or IL-6 promoted the differentiation of Th17 cells, and their combination resulted in further increase of the differentiation of Th17 cells, while IFN-γ and IL-12 reduced the percentages of Th17 cells. Moreover, these two cytokines significantly impaired the promotive effect induced by IL-1β plus IL-6.
Conclusion:
This study showed that Th1/Th17 balance existed in tuberculous pleural effusion, and was mainly due to the generation and differentiation of Th17 cells induced by IL-1β and IL-6, but reversed by IFN-γ and IL-12 in tuberculous pleural effusion.
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