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. 2020 Oct 14;10:17178. doi: 10.1038/s41598-020-73989-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed summarizing model. T_H1 cell-derived IL-26 is increased expressed in lymph node in tuberculosis patients. IL-26 shows direct antimycobacterial activity. This activity which is possible mediated via binding of IL-26 to mycobacterial surface molecule LAM. Besides direct activity against mycobacteria, IL-26 also improves intracellular killing of mycobacteria in THP1 macrophages. Furthermore, IL-26 induces cytokines such as TNF-α and chemokines such as CCL20, CXCL8 and CXCL2 in macrophages. CCL20 leads then to the further recruitment of T cells to the side of infection and CXCL8 as well as CXCL2 are attracting neutrophils.