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The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation

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The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation. / Sparber, Florian; De Gregorio, Corinne; Steckholzer, Simone; Ferreira, Filipa M; Dolowschiak, Tamas; Ruchti, Fiorella; Kirchner, Florian R; Mertens, Sarah; Prinz, Immo; Joller, Nicole; Buch, Thorsten; Glatz, Martin; Sallusto, Federica; LeibundGut-Landmann, Salomé.

In: CELL HOST MICROBE, Vol. 25, No. 3, 13.03.2019, p. 389-403.e6.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Sparber, F, De Gregorio, C, Steckholzer, S, Ferreira, FM, Dolowschiak, T, Ruchti, F, Kirchner, FR, Mertens, S, Prinz, I, Joller, N, Buch, T, Glatz, M, Sallusto, F & LeibundGut-Landmann, S 2019, 'The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation', CELL HOST MICROBE, vol. 25, no. 3, pp. 389-403.e6. https://doi.org/10.1016/j.chom.2019.02.002

APA

Sparber, F., De Gregorio, C., Steckholzer, S., Ferreira, F. M., Dolowschiak, T., Ruchti, F., Kirchner, F. R., Mertens, S., Prinz, I., Joller, N., Buch, T., Glatz, M., Sallusto, F., & LeibundGut-Landmann, S. (2019). The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation. CELL HOST MICROBE, 25(3), 389-403.e6. https://doi.org/10.1016/j.chom.2019.02.002

Vancouver

Sparber F, De Gregorio C, Steckholzer S, Ferreira FM, Dolowschiak T, Ruchti F et al. The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation. CELL HOST MICROBE. 2019 Mar 13;25(3):389-403.e6. https://doi.org/10.1016/j.chom.2019.02.002

Bibtex

@article{2f9a18dd10d043a8abd57fef996afd37,
title = "The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation",
abstract = "Commensal fungi of the mammalian skin, such as those of the genus Malassezia, are associated with atopic dermatitis and other common inflammatory skin disorders. Understanding of the causative relationship between fungal commensalism and disease manifestation remains incomplete. By developing a murine epicutaneous infection model, we found Malassezia spp. selectively induce IL-17 and related cytokines. This response is key in preventing fungal overgrowth on the skin, as disruption of the IL-23-IL-17 axis compromises Malassezia-specific cutaneous immunity. Under conditions of impaired skin integrity, mimicking a hallmark of atopic dermatitis, the presence of Malassezia dramatically aggravates cutaneous inflammation, which again was IL-23 and IL-17 dependent. Consistently, we found a CCR6+ Th17 subset of memory T cells to be Malassezia specific in both healthy individuals and atopic dermatitis patients, whereby the latter showed enhanced frequency of these cells. Thus, the Malassezia-induced type 17 response is pivotal in orchestrating antifungal immunity and in actively promoting skin inflammation.",
keywords = "Adult, Animals, Cytokines/metabolism, Dermatitis, Atopic/pathology, Dermatomycoses/microbiology, Disease Models, Animal, Female, Humans, Malassezia/immunology, Male, Mice, Inbred C57BL, Middle Aged, Th17 Cells/immunology, Young Adult",
author = "Florian Sparber and {De Gregorio}, Corinne and Simone Steckholzer and Ferreira, {Filipa M} and Tamas Dolowschiak and Fiorella Ruchti and Kirchner, {Florian R} and Sarah Mertens and Immo Prinz and Nicole Joller and Thorsten Buch and Martin Glatz and Federica Sallusto and Salom{\'e} LeibundGut-Landmann",
note = "Copyright {\textcopyright} 2019 Elsevier Inc. All rights reserved.",
year = "2019",
month = mar,
day = "13",
doi = "10.1016/j.chom.2019.02.002",
language = "English",
volume = "25",
pages = "389--403.e6",
journal = "CELL HOST MICROBE",
issn = "1931-3128",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation

AU - Sparber, Florian

AU - De Gregorio, Corinne

AU - Steckholzer, Simone

AU - Ferreira, Filipa M

AU - Dolowschiak, Tamas

AU - Ruchti, Fiorella

AU - Kirchner, Florian R

AU - Mertens, Sarah

AU - Prinz, Immo

AU - Joller, Nicole

AU - Buch, Thorsten

AU - Glatz, Martin

AU - Sallusto, Federica

AU - LeibundGut-Landmann, Salomé

N1 - Copyright © 2019 Elsevier Inc. All rights reserved.

PY - 2019/3/13

Y1 - 2019/3/13

N2 - Commensal fungi of the mammalian skin, such as those of the genus Malassezia, are associated with atopic dermatitis and other common inflammatory skin disorders. Understanding of the causative relationship between fungal commensalism and disease manifestation remains incomplete. By developing a murine epicutaneous infection model, we found Malassezia spp. selectively induce IL-17 and related cytokines. This response is key in preventing fungal overgrowth on the skin, as disruption of the IL-23-IL-17 axis compromises Malassezia-specific cutaneous immunity. Under conditions of impaired skin integrity, mimicking a hallmark of atopic dermatitis, the presence of Malassezia dramatically aggravates cutaneous inflammation, which again was IL-23 and IL-17 dependent. Consistently, we found a CCR6+ Th17 subset of memory T cells to be Malassezia specific in both healthy individuals and atopic dermatitis patients, whereby the latter showed enhanced frequency of these cells. Thus, the Malassezia-induced type 17 response is pivotal in orchestrating antifungal immunity and in actively promoting skin inflammation.

AB - Commensal fungi of the mammalian skin, such as those of the genus Malassezia, are associated with atopic dermatitis and other common inflammatory skin disorders. Understanding of the causative relationship between fungal commensalism and disease manifestation remains incomplete. By developing a murine epicutaneous infection model, we found Malassezia spp. selectively induce IL-17 and related cytokines. This response is key in preventing fungal overgrowth on the skin, as disruption of the IL-23-IL-17 axis compromises Malassezia-specific cutaneous immunity. Under conditions of impaired skin integrity, mimicking a hallmark of atopic dermatitis, the presence of Malassezia dramatically aggravates cutaneous inflammation, which again was IL-23 and IL-17 dependent. Consistently, we found a CCR6+ Th17 subset of memory T cells to be Malassezia specific in both healthy individuals and atopic dermatitis patients, whereby the latter showed enhanced frequency of these cells. Thus, the Malassezia-induced type 17 response is pivotal in orchestrating antifungal immunity and in actively promoting skin inflammation.

KW - Adult

KW - Animals

KW - Cytokines/metabolism

KW - Dermatitis, Atopic/pathology

KW - Dermatomycoses/microbiology

KW - Disease Models, Animal

KW - Female

KW - Humans

KW - Malassezia/immunology

KW - Male

KW - Mice, Inbred C57BL

KW - Middle Aged

KW - Th17 Cells/immunology

KW - Young Adult

U2 - 10.1016/j.chom.2019.02.002

DO - 10.1016/j.chom.2019.02.002

M3 - SCORING: Journal article

C2 - 30870621

VL - 25

SP - 389-403.e6

JO - CELL HOST MICROBE

JF - CELL HOST MICROBE

SN - 1931-3128

IS - 3

ER -