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The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation. / Minns, Danielle; Smith, Katie; Alessandrini, Virginia et al.
In: Nature Communications, Vol. 12, 1285, 24.02.2021.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Minns, D, Smith, K, Alessandrini, V, Hardisty, G, Melrose, L, Jackson-Jones, L, MacDonald, AS, Davidson, D & Gwyer Findlay, E 2021, 'The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation', Nature Communications, vol. 12, 1285. https://doi.org/10.1038/s41467-021-21533-5

APA

Minns, D., Smith, K., Alessandrini, V., Hardisty, G., Melrose, L., Jackson-Jones, L., MacDonald, A. S., Davidson, D., & Gwyer Findlay, E. (2021). The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation. Nature Communications, 12, Article 1285. https://doi.org/10.1038/s41467-021-21533-5

Vancouver

Minns D, Smith K, Alessandrini V, Hardisty G, Melrose L, Jackson-Jones L et al. The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation. Nature Communications. 2021 Feb 24;12:1285. doi: 10.1038/s41467-021-21533-5

Author

Minns, Danielle ; Smith, Katie ; Alessandrini, Virginia et al. / The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation. In: Nature Communications. 2021 ; Vol. 12.

Bibtex

@article{8081bfc984ac497fbfa642b972632db4,
title = "The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation",
abstract = "The host defence peptide cathelicidin (LL-37 in humans, mCRAMP in mice) is released from neutrophils by de-granulation, NETosis and necrotic death; it has potent anti-pathogen activity as well as being a broad immunomodulator. Here we report that cathelicidin is a powerful Th17 potentiator which enhances aryl hydrocarbon receptor (AHR) and RORγt expression, in a TGF-β1-dependent manner. In the presence of TGF-β1, cathelicidin enhanced SMAD2/3 and STAT3 phosphorylation, and profoundly suppressed IL-2 and T-bet, directing T cells away from Th1 and into a Th17 phenotype. Strikingly, Th17 but not Th1 cells were protected from apoptosis by cathelicidin. We show that cathelicidin is released by neutrophils in mouse lymph nodes and that cathelicidin-deficient mice display suppressed Th17 responses during inflammation, but not at steady state. We propose that the neutrophil cathelicidin is required for maximal Th17 differentiation, and that this is one method by which early neutrophilia directs subsequent adaptive immune responses.",
author = "Danielle Minns and Katie Smith and Virginia Alessandrini and Gareth Hardisty and Lauren Melrose and Lucy Jackson-Jones and MacDonald, {Andrew S} and Donald Davidson and {Gwyer Findlay}, Emily",
year = "2021",
month = feb,
day = "24",
doi = "10.1038/s41467-021-21533-5",
language = "English",
volume = "12",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation

AU - Minns, Danielle

AU - Smith, Katie

AU - Alessandrini, Virginia

AU - Hardisty, Gareth

AU - Melrose, Lauren

AU - Jackson-Jones, Lucy

AU - MacDonald, Andrew S

AU - Davidson, Donald

AU - Gwyer Findlay, Emily

PY - 2021/2/24

Y1 - 2021/2/24

N2 - The host defence peptide cathelicidin (LL-37 in humans, mCRAMP in mice) is released from neutrophils by de-granulation, NETosis and necrotic death; it has potent anti-pathogen activity as well as being a broad immunomodulator. Here we report that cathelicidin is a powerful Th17 potentiator which enhances aryl hydrocarbon receptor (AHR) and RORγt expression, in a TGF-β1-dependent manner. In the presence of TGF-β1, cathelicidin enhanced SMAD2/3 and STAT3 phosphorylation, and profoundly suppressed IL-2 and T-bet, directing T cells away from Th1 and into a Th17 phenotype. Strikingly, Th17 but not Th1 cells were protected from apoptosis by cathelicidin. We show that cathelicidin is released by neutrophils in mouse lymph nodes and that cathelicidin-deficient mice display suppressed Th17 responses during inflammation, but not at steady state. We propose that the neutrophil cathelicidin is required for maximal Th17 differentiation, and that this is one method by which early neutrophilia directs subsequent adaptive immune responses.

AB - The host defence peptide cathelicidin (LL-37 in humans, mCRAMP in mice) is released from neutrophils by de-granulation, NETosis and necrotic death; it has potent anti-pathogen activity as well as being a broad immunomodulator. Here we report that cathelicidin is a powerful Th17 potentiator which enhances aryl hydrocarbon receptor (AHR) and RORγt expression, in a TGF-β1-dependent manner. In the presence of TGF-β1, cathelicidin enhanced SMAD2/3 and STAT3 phosphorylation, and profoundly suppressed IL-2 and T-bet, directing T cells away from Th1 and into a Th17 phenotype. Strikingly, Th17 but not Th1 cells were protected from apoptosis by cathelicidin. We show that cathelicidin is released by neutrophils in mouse lymph nodes and that cathelicidin-deficient mice display suppressed Th17 responses during inflammation, but not at steady state. We propose that the neutrophil cathelicidin is required for maximal Th17 differentiation, and that this is one method by which early neutrophilia directs subsequent adaptive immune responses.

U2 - 10.1038/s41467-021-21533-5

DO - 10.1038/s41467-021-21533-5

M3 - Journal article

VL - 12

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 1285

ER -