IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells
Name
nihms-1531938.pdf
Description
Accepted version
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982.15 KB
Format
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Checksum (MD5)
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Author(s)
Weiss, David I
Ma, Feiyang
Merleev, Alexander A
Maverakis, Emanual
Gilliet, Michel
Balin, Samuel J
Bryson, Bryan D
Ochoa, Maria Teresa
Pellegrini, Matteo
Bloom, Barry R
Date Issued
2019
Journal
Journal of immunology
Publisher
The American Association of Immunologists
Version
Author's final manuscript
Abstract
© 2019 by The American Association of Immunologists, Inc. Th17 cells play a critical role in the adaptive immune response against extracellular bacteria, and the possible mechanisms by which they can protect against infection are of particular interest. In this study, we describe, to our knowledge, a novel IL-1b dependent pathway for secretion of the antimicrobial peptide IL-26 from human Th17 cells that is independent of and more rapid than classical TCR activation. We find that IL-26 is secreted 3 hours after treating PBMCs with Mycobacterium leprae as compared with 48 hours for IFN-g and IL-17A. IL-1b was required for microbial ligand induction of IL-26 and was sufficient to stimulate IL-26 release from Th17 cells. Only IL-1RI+ Th17 cells responded to IL-1b, inducing an NF-kB–regulated transcriptome. Finally, supernatants from IL-1b–treated memory T cells killed Escherichia coli in an IL-26–dependent manner. These results identify a mechanism by which human IL-1RI+ “antimicrobial Th17 cells” can be rapidly activated by IL-1b as part of the innate immune response to produce IL-26 to kill extracellular bacteria.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
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Creative Commons Attribution-Noncommercial-Share Alike
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DOI of Published Version
https://doi.org/10.4049/JIMMUNOL.1900318
