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Interleukin-26 upregulates interleukin-22 production by human CD4+ T cells in tuberculous pleurisy

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Abstract

IL-26 is a potentially important player in host defense and may be a pathogenic factor in the chronic inflammatory disorders of humans. However, the involvement of IL-26 in tuberculous pleural effusion (TPE) has not been investigated. The concentration of IL-26 was determined in pleural fluids and sera from patients with pleural effusions. Flow cytometry was performed to identify the cell origin of IL-26. The effects of tuberculosis-specific antigen (ESAT-6/CFP-10) on IL-26 expression of CD4+ T cell were explored. The impacts of IL-26 on modulating CD4+ T cell polarization were also investigated. The concentrations of IL-26 were much higher in tuberculous, malignant, and infectious PE than those in the corresponding serum. The expression of IL-26 on CD4+ T cells was much higher in tuberculous PE than those in the corresponding serum, and pleural Th1 and Th17 cells might be the major cell sources of IL-26. The addition of ESAT-6/CFP-10 to CD4+ T cells led to increasing the number of IL-26–producing CD4+ T cells and IL-26 expression on Th1 and Th17 cells. IL-26 could induce the differentiation and generation of IL-22 by memory and naive CD4+ T cells. IL-26 also upregulated the mRNA encoding CC-chemokine ligand 20 (CCL20) and CCL22 by mononuclear cells isolated from TPE. This study implies that pleural Th1 and Th17 cells are the major cell sources of IL-26, which could induce the differentiation and generation of Th22 cells by CD4+ T cells, suggesting the involvement of IL-26 in the pathogenesis of human TPE.

Key messages

  • IL-26 is overexpressed in TPE patients and presents a higher concentration in pleural effusion than the corresponding peripheral blood.

  • Pleural Th1 and Th17 cells might be the major cell sources of IL-26 in TPE patients.

  • IL-26 promotes IL-22 secretion and Th22 generation by CD4+ T cells isolated from TPE patients.

  • IL-26 may play an active role in the pathogenesis of tuberculous pleurisy.

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Funding

This work was supported in part by grants from the National Natural Science Foundation of China (No. 81770090 and No. 81470274).

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Correspondence to Qiong Zhou.

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The Ethics Committee of Tongji Medical College, Huazhong University of Science and Technology approved the study protocol.

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Zhang, M., Niu, YR., Liu, JY. et al. Interleukin-26 upregulates interleukin-22 production by human CD4+ T cells in tuberculous pleurisy. J Mol Med 97, 619–631 (2019). https://doi.org/10.1007/s00109-018-01741-1

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  • DOI: https://doi.org/10.1007/s00109-018-01741-1

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