| Title: |
IL-1β Induces the Rapid Secretion of the Antimicrobial Protein IL-26 from Th17 Cells. |
| Authors: |
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 |
| Source: |
The Journal of Immunology, vol 203, iss 4 |
| Publisher Information: |
eScholarship, University of California |
| Publication Year: |
2019 |
| Collection: |
University of California: eScholarship |
| Subject Terms: |
3207 Medical Microbiology (for-2020); 32 Biomedical and Clinical Sciences (for-2020); 31 Biological Sciences (for-2020); 3204 Immunology (for-2020); Biodefense (rcdc); Infectious Diseases (rcdc); Emerging Infectious Diseases (rcdc); 1.1 Normal biological development and functioning (hrcs-rac); Infection (hrcs-hc); Bacterial Infections (mesh); Humans (mesh); Immunity; Innate (mesh); Interleukin-1beta (mesh); Interleukins (mesh); Lymphocyte Activation (mesh); Th17 Cells (mesh); 1107 Immunology (for); Immunology (science-metrix); 3101 Biochemistry and cell biology (for-2020) |
| Subject Geographic: |
911 - 921 |
| Description: |
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-1β 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-γ and IL-17A. IL-1β 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-1β, inducing an NF-κB-regulated transcriptome. Finally, supernatants from IL-1β-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-1β as part of the innate immune response to produce IL-26 to kill extracellular bacteria. |
| Document Type: |
article in journal/newspaper |
| File Description: |
application/pdf |
| Language: |
unknown |
| Relation: |
qt1hv887n9; https://escholarship.org/uc/item/1hv887n9; https://escholarship.org/content/qt1hv887n9/qt1hv887n9.pdf |
| DOI: |
10.4049/jimmunol.1900318 |
| Availability: |
https://escholarship.org/uc/item/1hv887n9; https://escholarship.org/content/qt1hv887n9/qt1hv887n9.pdf; https://doi.org/10.4049/jimmunol.1900318 |
| Rights: |
public |
| Accession Number: |
edsbas.2F22C763 |
| Database: |
BASE |