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IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis

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IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis. / Burstein, Verónica L; Guasconi, Lorena; Beccacece, Ignacio; Theumer, Martin G; Mena, Cristian; Prinz, Immo; Cervi, Laura; Herrero, Mónica; Masih, Diana T; Chiapello, Laura S.

in: J INVEST DERMATOL, Jahrgang 138, Nr. 8, 08.2018, S. 1744-1753.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Burstein, VL, Guasconi, L, Beccacece, I, Theumer, MG, Mena, C, Prinz, I, Cervi, L, Herrero, M, Masih, DT & Chiapello, LS 2018, 'IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis', J INVEST DERMATOL, Jg. 138, Nr. 8, S. 1744-1753. https://doi.org/10.1016/j.jid.2018.02.042

APA

Burstein, V. L., Guasconi, L., Beccacece, I., Theumer, M. G., Mena, C., Prinz, I., Cervi, L., Herrero, M., Masih, D. T., & Chiapello, L. S. (2018). IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis. J INVEST DERMATOL, 138(8), 1744-1753. https://doi.org/10.1016/j.jid.2018.02.042

Vancouver

Burstein VL, Guasconi L, Beccacece I, Theumer MG, Mena C, Prinz I et al. IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis. J INVEST DERMATOL. 2018 Aug;138(8):1744-1753. https://doi.org/10.1016/j.jid.2018.02.042

Bibtex

@article{ab471f7b63574c39acf95c4c800a145f,
title = "IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis",
abstract = "Despite worldwide prevalence of superficial mycoses, the immune response in dermatophytosis has scarcely been investigated. In this study, we developed a model of superficial skin infection in C57BL/6 mice with Microsporum canis, a highly prevalent human pathogen. This model mimics mild inflammatory human dermatophytosis, characterized by neutrophil recruitment and fungal invasion limited to the epidermis and exhibits the establishment of a specific T helper type 17 immune response during infection. By using IL-17RA- or IL-17A/F-deficient mice we showed that, in the absence of a functional IL-17 pathway, M. canis extensively colonizes the epidermis and promotes an exaggerated skin inflammation and a shift to an IFN-γ-mediated (T helper type 1) response. IL-17 signaling was not involved in neutrophil influx to skin or fungal invasion to deeper tissues. Finally, this study shows that skin langerin-expressing cells contribute to the antifungal T helper type 17 response in vivo. In conclusion, these data directly show a dual function of IL-17 cytokines in dermatophytosis by controlling superficial infection and down-modulating a T helper type 1 antifungal response.",
keywords = "Animals, Disease Models, Animal, Epidermis/immunology, Host-Pathogen Interactions/immunology, Humans, Interleukin-17/genetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Microsporum/immunology, Neutrophil Infiltration/immunology, Receptors, Interleukin-17/genetics, Signal Transduction/immunology, Th17 Cells/immunology, Tinea/immunology",
author = "Burstein, {Ver{\'o}nica L} and Lorena Guasconi and Ignacio Beccacece and Theumer, {Martin G} and Cristian Mena and Immo Prinz and Laura Cervi and M{\'o}nica Herrero and Masih, {Diana T} and Chiapello, {Laura S}",
note = "Copyright {\textcopyright} 2018 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = aug,
doi = "10.1016/j.jid.2018.02.042",
language = "English",
volume = "138",
pages = "1744--1753",
journal = "J INVEST DERMATOL",
issn = "0022-202X",
publisher = "NATURE PUBLISHING GROUP",
number = "8",

}

RIS

TY - JOUR

T1 - IL-17-Mediated Immunity Controls Skin Infection and T Helper 1 Response during Experimental Microsporum canis Dermatophytosis

AU - Burstein, Verónica L

AU - Guasconi, Lorena

AU - Beccacece, Ignacio

AU - Theumer, Martin G

AU - Mena, Cristian

AU - Prinz, Immo

AU - Cervi, Laura

AU - Herrero, Mónica

AU - Masih, Diana T

AU - Chiapello, Laura S

N1 - Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/8

Y1 - 2018/8

N2 - Despite worldwide prevalence of superficial mycoses, the immune response in dermatophytosis has scarcely been investigated. In this study, we developed a model of superficial skin infection in C57BL/6 mice with Microsporum canis, a highly prevalent human pathogen. This model mimics mild inflammatory human dermatophytosis, characterized by neutrophil recruitment and fungal invasion limited to the epidermis and exhibits the establishment of a specific T helper type 17 immune response during infection. By using IL-17RA- or IL-17A/F-deficient mice we showed that, in the absence of a functional IL-17 pathway, M. canis extensively colonizes the epidermis and promotes an exaggerated skin inflammation and a shift to an IFN-γ-mediated (T helper type 1) response. IL-17 signaling was not involved in neutrophil influx to skin or fungal invasion to deeper tissues. Finally, this study shows that skin langerin-expressing cells contribute to the antifungal T helper type 17 response in vivo. In conclusion, these data directly show a dual function of IL-17 cytokines in dermatophytosis by controlling superficial infection and down-modulating a T helper type 1 antifungal response.

AB - Despite worldwide prevalence of superficial mycoses, the immune response in dermatophytosis has scarcely been investigated. In this study, we developed a model of superficial skin infection in C57BL/6 mice with Microsporum canis, a highly prevalent human pathogen. This model mimics mild inflammatory human dermatophytosis, characterized by neutrophil recruitment and fungal invasion limited to the epidermis and exhibits the establishment of a specific T helper type 17 immune response during infection. By using IL-17RA- or IL-17A/F-deficient mice we showed that, in the absence of a functional IL-17 pathway, M. canis extensively colonizes the epidermis and promotes an exaggerated skin inflammation and a shift to an IFN-γ-mediated (T helper type 1) response. IL-17 signaling was not involved in neutrophil influx to skin or fungal invasion to deeper tissues. Finally, this study shows that skin langerin-expressing cells contribute to the antifungal T helper type 17 response in vivo. In conclusion, these data directly show a dual function of IL-17 cytokines in dermatophytosis by controlling superficial infection and down-modulating a T helper type 1 antifungal response.

KW - Animals

KW - Disease Models, Animal

KW - Epidermis/immunology

KW - Host-Pathogen Interactions/immunology

KW - Humans

KW - Interleukin-17/genetics

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Microsporum/immunology

KW - Neutrophil Infiltration/immunology

KW - Receptors, Interleukin-17/genetics

KW - Signal Transduction/immunology

KW - Th17 Cells/immunology

KW - Tinea/immunology

U2 - 10.1016/j.jid.2018.02.042

DO - 10.1016/j.jid.2018.02.042

M3 - SCORING: Journal article

C2 - 29571944

VL - 138

SP - 1744

EP - 1753

JO - J INVEST DERMATOL

JF - J INVEST DERMATOL

SN - 0022-202X

IS - 8

ER -