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dc.contributor.authorHawerkamp, Heike C.
dc.contributor.authorvan Geelen, Lasse
dc.contributor.authorKorte, Jan
dc.contributor.authorDi Domizio, Jeremy
dc.contributor.authorSwidergall, Marc
dc.contributor.authorMomin, Afaque Ahmad Imtiyaz
dc.contributor.authorGuzmán-Vega, Francisco J.
dc.contributor.authorArold, Stefan T.
dc.contributor.authorErnst, Joachim
dc.contributor.authorGilliet, Michel
dc.contributor.authorKalscheuer, Rainer
dc.contributor.authorHomey, Bernhard
dc.contributor.authorMeller, Stephan
dc.date.accessioned2020-10-15T11:50:49Z
dc.date.available2020-10-15T11:50:49Z
dc.date.issued2020-10-14
dc.date.submitted2019-03-27
dc.identifier.citationHawerkamp, H. C., van Geelen, L., Korte, J., Di Domizio, J., Swidergall, M., Momin, A. A., … Meller, S. (2020). Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis. Scientific Reports, 10(1). doi:10.1038/s41598-020-73989-y
dc.identifier.issn2045-2322
dc.identifier.doi10.1038/s41598-020-73989-y
dc.identifier.urihttp://hdl.handle.net/10754/665596
dc.description.abstractAbstract Tuberculosis-causing Mycobacterium tuberculosis (Mtb) is transmitted via airborne droplets followed by a primary infection of macrophages and dendritic cells. During the activation of host defence mechanisms also neutrophils and T helper 1 (TH1) and TH17 cells are recruited to the site of infection. The TH17 cell-derived interleukin (IL)-17 in turn induces the cathelicidin LL37 which shows direct antimycobacterial effects. Here, we investigated the role of IL-26, a TH1- and TH17-associated cytokine that exhibits antimicrobial activity. We found that both IL-26 mRNA and protein are strongly increased in tuberculous lymph nodes. Furthermore, IL-26 is able to directly kill Mtb and decrease the infection rate in macrophages. Binding of IL-26 to lipoarabinomannan might be one important mechanism in extracellular killing of Mtb. Macrophages and dendritic cells respond to IL-26 with secretion of tumor necrosis factor (TNF)-α and chemokines such as CCL20, CXCL2 and CXCL8. In dendritic cells but not in macrophages cytokine induction by IL-26 is partly mediated via Toll like receptor (TLR) 2. Taken together, IL-26 strengthens the defense against Mtb in two ways: firstly, directly due to its antimycobacterial properties and secondly indirectly by activating innate immune mechanisms.
dc.description.sponsorshipWe thank S. Köhler from the Center for Advanced Imaging, Heinrich-Heine-University Düsseldorf for performing SEM. We further thank H. Mayringer, N. Simiantonaki and I. Esposito from the Institute of Pathology, Medical Faculty, Heinrich-Heine-University Düsseldorf for providing FFPE-lymph node sections from healthy individuals and tuberculosis patients. S. Meller was supported by the Stettendorf Stiftung.
dc.description.sponsorshipOpen Access funding enabled and organized by Projekt DEAL.
dc.publisherSpringer Science and Business Media LLC
dc.relation.urlhttp://www.nature.com/articles/s41598-020-73989-y
dc.rightsThis 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.
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleInterleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis
dc.typeArticle
dc.contributor.departmentBioscience Program
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentDivision of Biological and Environmental Sciences and Engineering (BESE), Computational Bioscience Research Center (CBRC), King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia.
dc.contributor.departmentComputational Bioscience Research Center (CBRC)
dc.contributor.departmentComputer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
dc.identifier.journalScientific Reports
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionDepartment of Dermatology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
dc.contributor.institutionDepartment of Pharmaceutical Biology and Biotechnology, Heinrich-Heine-University, Düsseldorf, Germany.
dc.contributor.institutionDepartment of Dermatology, University Hospital CHUV, Lausanne, Switzerland.
dc.contributor.institutionDepartment of Biology, Molecular Mycology, Heinrich-Heine-University, Düsseldorf, Germany.
dc.identifier.volume10
dc.identifier.issue1
kaust.personMomin, Afaque Ahmad Imtiyaz
kaust.personGuzmán-Vega, Francisco J.
kaust.personArold, Stefan T.
dc.date.accepted2020-08-31
refterms.dateFOA2020-10-15T11:52:02Z


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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.
Except where otherwise noted, this item's license is described as 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.