Interleukin-16 in tuberculous and malignant pleural effusions

Xj, Qin; Hz, Shi; Zx, Huang; Lf, Kang; Wn, Mo; Wu, Chao

doi:10.1183/09031936.05.00090804

Cited by 33 publications

(16 citation statements)

References 36 publications

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“…We speculated that an increased percentage of Th17 cells in MPE might be due to local differentiation and/or active recruitment. In the previous study, we provided direct evidence that IL-16 is capable of inducing CD4 + T cell infiltration into the pleural space (33). Therefore, as a subpopulation of CD4 + T cells, Th17 cells might also be recruited in to MPE by local production of IL-16, because IL-16 level is significantly higher in MPE than in serum (33).…”

Section: Discussionmentioning

confidence: 83%

Generation and Differentiation of IL-17–Producing CD4+ T Cells in Malignant Pleural Effusion

Zhou

et al. 2010

The Journal of Immunology

130

106

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IL-17–producing CD4+ T (Th17) cells have been found to be increased in some human cancers; however, the possible implication of Th17 cells in regulating antitumor responses in malignant pleural effusion (MPE) remains to be elucidated. In the current study, distribution and phenotypic features of Th17 cells in both MPE and peripheral blood from patients with lung cancer were determined by flow cytometry or double immunofluorescence staining. The impacts of cytokines on Th17 cell generation and differentiation were explored. The chemoattractant activity of chemokines CCL20 and CCL22 for Th17 cells in vitro was also observed. It was found that the increased Th17 cells could be found in MPE compared with blood. The in vitro experiments showed that IL-1β, IL-6, IL-23, or their various combinations could promote Th17 cell generation and differentiation from naive CD4+ T cells. MPE was chemotactic for Th17 cells, and this activity was partly blocked by anti-CCL20 and/or CCL22 Abs. Our data also showed that the accumulation of Th17 cells in MPE predicted improved patient survival. It could be concluded that the overrepresentation of Th17 cells in MPE might be due to Th17 cell differentiation and expansion stimulated by pleural proinflammatory cytokines and to recruitment of Th17 cells from peripheral blood induced by pleural chemokines CCL20 and CCL22. Furthermore, the accumulation of Th17 cells in MPE predicted improved patient survival. These data provide the basis for developing immune-boosting strategies based on ridding the cancer patient of this cell population.

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Section: Discussionmentioning

confidence: 83%

Generation and Differentiation of IL-17–Producing CD4+ T Cells in Malignant Pleural Effusion

Zhou

et al. 2010

The Journal of Immunology

130

106

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“…This migration of Treg cells from host tissues into the developing mesotheliomas was demonstrated in a study using a murine model where mesothelioma cells were implanted intra-peritoneally into GFP-expressing mice [23]. CCL24, which recruits resting T cells [24], and interleukin (IL)-16, which has previously been shown in malignant pleural effusions to attract and assist in the differentiation of Treg cells [25], were both found to be upregulated 7 days post tumour implantation. In addition, macrophage derived CCL17 and CCL22, known to recruit and assist in the differentiation of Treg cells, were shown to peak at day 14 post tumour challenge suggesting that macrophages may also play an important role in Treg cell recruitment to mesotheliomas.…”

Section: Recruitment Of Treg Cells To Mesotheliomasmentioning

confidence: 99%

The Role of Regulatory T Cells in Mesothelioma

Ireland

Beilharz

2012

Cancer Microenvironment

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Malignant mesothelioma (MM) appears to be responsive to immunotherapy. The lack of complete tumour cure as a result of many immunotherapies tested to date suggests that the immune response to MM is complex and multi-parametric. Regulatory T (Treg) cells are prevalent within murine and human mesotheliomas with their removal shown to result in tumour growth inhibition and the release of anti-tumour effector T cells from immunosuppression. The targeting of immune checkpoints as treatments for various solid tumours has recently shown promise in clinical settings. In addition, synergy between chemotherapy and immunotherapy has been demonstrated for many cancers, including mesothelioma. Here we demonstrate Treg cells as critical mediators of the anti-tumour immune response to MM and potential targets for anti-tumour immunotherapy; though the timing and dosage of Treg cell manipulating immunotherapies need to be optimised.

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“…Certain cytokines and chemokines released by activated inflammatory cells, particularly T lymphocytes and macrophages, are responsible for this process (2). By contrast, malignant pleural effusions (MPEs) are primarily caused by pleural metastasis or lymphatic obstruction and are diagnosed by the presence of malignant cells on the pleura or in the effusions (3). Cytokines, including interferon (IFN)-γ and interleukin (IL)-1, -6, -16 and -17 have shown diagnostic, differential and prognostic significance in TPEs and MPEs (1–3).…”

Section: Introductionmentioning

confidence: 99%

“…By contrast, malignant pleural effusions (MPEs) are primarily caused by pleural metastasis or lymphatic obstruction and are diagnosed by the presence of malignant cells on the pleura or in the effusions (3). Cytokines, including interferon (IFN)-γ and interleukin (IL)-1, -6, -16 and -17 have shown diagnostic, differential and prognostic significance in TPEs and MPEs (1–3). These findings indicate that the activation of lymphocytes and the release of cytokines may have important roles in the development of TPEs and MPEs.…”

Section: Introductionmentioning

confidence: 99%

IL-33 levels differentiate tuberculous pleurisy from malignant pleural effusions

et al. 2014

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Tuberculous pleural effusions (TPEs) and malignant pleural effusions (MPEs) are difficult to differentiate between in certain clinical situations. Interleukin (IL)-33 is a cytokine that participates in inflammatory responses and may have a role in pleural effusions. The present study aimed to investigate the concentrations and potential differential significance of IL-33 in patients with TPE and MPE. IL-33 levels in pleural effusion and serum samples were detected using sandwich enzyme-linked immunosorbent assay in 23 patients with TPE and 21 patients with MPE. The concentration of IL-33 (mean ± standard deviation) in the TPE patients (22.962±0.976 ng/l) was significantly higher than that in the MPE patients (12.603±5.153 ng/l; P<0.001; z=−4.572); however, there was no significant difference in the serum level of IL-33 in the patients with TPE compared with those with MPE (P>0.05). The concentration of IL-33 in the pleural effusions was positively correlated with that in the serum samples in each group (TPE: r=0.563, P=0.05; MPE: r=0.535, P<0.05). The cut-off value of pleural IL-33 for TPE was 19.86 ng/l, which yielded a sensitivity of 0.869, a specificity of 0.905 and an area under the corresponding receiver operating characteristic curve of 0.903. The present study identified that the level of pleural IL-33 is significantly increased in TPEs and may serve as a novel biomarker to differentiate between patients with TPE and MPE.

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Interleukin-16 in tuberculous and malignant pleural effusions

Cited by 33 publications

References 36 publications

Generation and Differentiation of IL-17–Producing CD4+ T Cells in Malignant Pleural Effusion

Generation and Differentiation of IL-17–Producing CD4+ T Cells in Malignant Pleural Effusion

The Role of Regulatory T Cells in Mesothelioma

IL-33 levels differentiate tuberculous pleurisy from malignant pleural effusions

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