IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells
© 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,...
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| Format: | Article |
| Language: | English |
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The American Association of Immunologists
2021
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| Online Access: | https://hdl.handle.net/1721.1/136146 |
| _version_ | 1826215065991249920 |
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| author | 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 Modlin, Robert L |
| author2 | Massachusetts Institute of Technology. Department of Biological Engineering |
| author_facet | Massachusetts Institute of Technology. Department of Biological Engineering 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 Modlin, Robert L |
| author_sort | Weiss, David I |
| collection | MIT |
| description | © 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. |
| first_indexed | 2024-09-23T16:16:00Z |
| format | Article |
| id | mit-1721.1/136146 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T16:16:00Z |
| publishDate | 2021 |
| publisher | The American Association of Immunologists |
| record_format | dspace |
| spelling | mit-1721.1/1361462023-11-14T19:55:27Z IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells 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 Modlin, Robert L Massachusetts Institute of Technology. Department of Biological Engineering © 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. 2021-10-27T20:31:04Z 2021-10-27T20:31:04Z 2019 2021-08-25T17:08:18Z Article http://purl.org/eprint/type/JournalArticle https://hdl.handle.net/1721.1/136146 en 10.4049/JIMMUNOL.1900318 Journal of immunology Creative Commons Attribution-Noncommercial-Share Alike http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf The American Association of Immunologists PMC |
| spellingShingle | 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 Modlin, Robert L IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title | IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title_full | IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title_fullStr | IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title_full_unstemmed | IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title_short | IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells |
| title_sort | il 1β induces the rapid secretion of the antimicrobial protein il 26 from th17 cells |
| url | https://hdl.handle.net/1721.1/136146 |
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