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High IL-35 pleural expression in patients with tuberculous pleural effusion
1Department of Respiratory Medicine, Zhongnan Hospital of Wuhan University No. 169, Wuhan, Hubei, China (mainland).
Summary
Interleukin-35 (IL-35) is elevated in tuberculous pleural effusion (TPE), suggesting an immune imbalance. This cytokine may play a role in TPE pathogenesis and could be a potential therapeutic target.
Area of Science:
- Immunology
- Respiratory Medicine
- Cytokine Research
Background:
- Interleukin-35 (IL-35) is an anti-inflammatory cytokine produced by regulatory T cells.
- Its role in inflammatory and autoimmune diseases is established, but its involvement in tuberculous pleural effusion (TPE) is unknown.
Purpose of the Study:
- To investigate the potential role of IL-35 in the pathogenesis of TPE.
- To compare IL-35 levels in TPE with malignant pleural effusion (MPE) and blood from TPE patients.
Main Methods:
- Analysis of pleural effusion and blood samples from TPE and MPE patients.
- Flow cytometry to quantify IL-35-producing cells and T cell subsets (Th1, Th17).
- Real-time RT-PCR, ELISA, and immunofluorescence to assess IL-35 expression and localization.
- ELISPOT assay to evaluate the functional impact of IL-35 on T cells.
Main Results:
- IL-35-producing cells were significantly higher in TPE compared to MPE and blood from TPE patients.
- Elevated levels of IL-35, IL-17, and IFN-γ were observed in TPE compared to MPE.
- IL-35 demonstrated an inhibitory effect on IFN-γ-producing CD4+ T cells in TPE.
- Higher IL-35 mRNA expression and presence of IL-35-positive cells in pleural tissues of TPE patients.
Conclusions:
- TPE exhibits an imbalance in IL-35 metabolism.
- IL-35 may contribute to the immune response in TPE.
- IL-35 warrants further investigation as a potential therapeutic target for TPE.
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