Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity

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Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity. / Christensen, Pernille Kristine Fisker; Hansen, Axel Kornerup; Skov, Søren; Martel, Britta Cathrina; Larsen, Jesper; Høyer-Hansen, Maria Helena; Koch, Janne.

In: PLoS ONE, Vol. 18, e0281005, 2023.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Christensen, PKF, Hansen, AK, Skov, S, Martel, BC, Larsen, J, Høyer-Hansen, MH & Koch, J 2023, 'Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity', PLoS ONE, vol. 18, e0281005. https://doi.org/10.1371/journal.pone.0281005

APA

Christensen, P. K. F., Hansen, A. K., Skov, S., Martel, B. C., Larsen, J., Høyer-Hansen, M. H., & Koch, J. (2023). Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity. PLoS ONE, 18, [e0281005]. https://doi.org/10.1371/journal.pone.0281005

Vancouver

Christensen PKF, Hansen AK, Skov S, Martel BC, Larsen J, Høyer-Hansen MH et al. Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity. PLoS ONE. 2023;18. e0281005. https://doi.org/10.1371/journal.pone.0281005

Author

Christensen, Pernille Kristine Fisker ; Hansen, Axel Kornerup ; Skov, Søren ; Martel, Britta Cathrina ; Larsen, Jesper ; Høyer-Hansen, Maria Helena ; Koch, Janne. / Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity. In: PLoS ONE. 2023 ; Vol. 18.

Bibtex

@article{5017a58442c042e6adf4238a2332e569,
title = "Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity",
abstract = "Human immune system (HIS) mouse models can be valuable when cross-reactivity of drug candidates to mouse systems is missing. However, no HIS mouse models of psoriasis have been established. In this study, it was investigated if imiquimod (IMQ) induced psoriasis-like skin inflammation was driven by human immune cells in human FMS-related tyrosine kinase 3 ligand (hFlt3L) boosted (BRGSF-HIS mice). BRGSF-HIS mice were boosted with hFlt3L prior to two or three topical applications of IMQ. Despite clinical skin inflammation, increased epidermal thickness and influx of human immune cells, a human derived response was not pronounced in IMQ treated mice. However, the number of murine neutrophils and murine cytokines and chemokines were increased in the skin and systemically after IMQ application. In conclusion, IMQ did induce skin inflammation in hFlt3L boosted BRGSF-HIS mice, although, a limited human immune response suggest that the main driving cellular mechanisms were of murine origin.",
author = "Christensen, {Pernille Kristine Fisker} and Hansen, {Axel Kornerup} and S{\o}ren Skov and Martel, {Britta Cathrina} and Jesper Larsen and H{\o}yer-Hansen, {Maria Helena} and Janne Koch",
note = "Publisher Copyright: Copyright: {\textcopyright} 2023 Christensen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.",
year = "2023",
doi = "10.1371/journal.pone.0281005",
language = "English",
volume = "18",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",

}

RIS

TY - JOUR

T1 - Imiquimod induces skin inflammation in humanized BRGSF mice with limited human immune cell activity

AU - Christensen, Pernille Kristine Fisker

AU - Hansen, Axel Kornerup

AU - Skov, Søren

AU - Martel, Britta Cathrina

AU - Larsen, Jesper

AU - Høyer-Hansen, Maria Helena

AU - Koch, Janne

N1 - Publisher Copyright: Copyright: © 2023 Christensen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PY - 2023

Y1 - 2023

N2 - Human immune system (HIS) mouse models can be valuable when cross-reactivity of drug candidates to mouse systems is missing. However, no HIS mouse models of psoriasis have been established. In this study, it was investigated if imiquimod (IMQ) induced psoriasis-like skin inflammation was driven by human immune cells in human FMS-related tyrosine kinase 3 ligand (hFlt3L) boosted (BRGSF-HIS mice). BRGSF-HIS mice were boosted with hFlt3L prior to two or three topical applications of IMQ. Despite clinical skin inflammation, increased epidermal thickness and influx of human immune cells, a human derived response was not pronounced in IMQ treated mice. However, the number of murine neutrophils and murine cytokines and chemokines were increased in the skin and systemically after IMQ application. In conclusion, IMQ did induce skin inflammation in hFlt3L boosted BRGSF-HIS mice, although, a limited human immune response suggest that the main driving cellular mechanisms were of murine origin.

AB - Human immune system (HIS) mouse models can be valuable when cross-reactivity of drug candidates to mouse systems is missing. However, no HIS mouse models of psoriasis have been established. In this study, it was investigated if imiquimod (IMQ) induced psoriasis-like skin inflammation was driven by human immune cells in human FMS-related tyrosine kinase 3 ligand (hFlt3L) boosted (BRGSF-HIS mice). BRGSF-HIS mice were boosted with hFlt3L prior to two or three topical applications of IMQ. Despite clinical skin inflammation, increased epidermal thickness and influx of human immune cells, a human derived response was not pronounced in IMQ treated mice. However, the number of murine neutrophils and murine cytokines and chemokines were increased in the skin and systemically after IMQ application. In conclusion, IMQ did induce skin inflammation in hFlt3L boosted BRGSF-HIS mice, although, a limited human immune response suggest that the main driving cellular mechanisms were of murine origin.

U2 - 10.1371/journal.pone.0281005

DO - 10.1371/journal.pone.0281005

M3 - Journal article

C2 - 36800344

AN - SCOPUS:85148297732

VL - 18

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

M1 - e0281005

ER -

ID: 337601258