Psoriasis Pathogenesis: Keratinocytes Are Back in the Spotlight

Natalie Garzorz-Stark; Kilian Eyerich

doi:10.1016/j.jid.2019.01.026

Psoriasis Pathogenesis: Keratinocytes Are Back in the Spotlight

Natalie Garzorz-Stark
, Kilian Eyerich

Department of Dermatology and Allergology

Technical University of Munich

Research output: Contribution to journal › Comment/debate

41 Scopus citations

Abstract

Psoriasis is a T helper type 17–mediated immune disease. Initial triggers that lead to T helper type 17 production and inflammatory cell recruitment into skin are being delineated. Autoantigens that stimulate T helper type 17 cells are also being identified. A new and important piece of the puzzle indicates that keratinocytes not only amplify inflammation, but that they are essential for a full-blown IL-17–mediated psoriatic phenotype in mice.

Original language	English
Pages (from-to)	995-996
Number of pages	2
Journal	Journal of Investigative Dermatology
Volume	139
Issue number	5
DOIs	https://doi.org/10.1016/j.jid.2019.01.026
State	Published - May 2019

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title = "Psoriasis Pathogenesis: Keratinocytes Are Back in the Spotlight",

abstract = "Psoriasis is a T helper type 17–mediated immune disease. Initial triggers that lead to T helper type 17 production and inflammatory cell recruitment into skin are being delineated. Autoantigens that stimulate T helper type 17 cells are also being identified. A new and important piece of the puzzle indicates that keratinocytes not only amplify inflammation, but that they are essential for a full-blown IL-17–mediated psoriatic phenotype in mice.",

author = "Natalie Garzorz-Stark and Kilian Eyerich",

note = "Publisher Copyright: {\textcopyright} 2019 The Authors",

year = "2019",

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TY - JOUR

T1 - Psoriasis Pathogenesis

T2 - Keratinocytes Are Back in the Spotlight

AU - Garzorz-Stark, Natalie

AU - Eyerich, Kilian

PY - 2019/5

Y1 - 2019/5

N2 - Psoriasis is a T helper type 17–mediated immune disease. Initial triggers that lead to T helper type 17 production and inflammatory cell recruitment into skin are being delineated. Autoantigens that stimulate T helper type 17 cells are also being identified. A new and important piece of the puzzle indicates that keratinocytes not only amplify inflammation, but that they are essential for a full-blown IL-17–mediated psoriatic phenotype in mice.

AB - Psoriasis is a T helper type 17–mediated immune disease. Initial triggers that lead to T helper type 17 production and inflammatory cell recruitment into skin are being delineated. Autoantigens that stimulate T helper type 17 cells are also being identified. A new and important piece of the puzzle indicates that keratinocytes not only amplify inflammation, but that they are essential for a full-blown IL-17–mediated psoriatic phenotype in mice.

UR - https://www.scopus.com/pages/publications/85064148849

U2 - 10.1016/j.jid.2019.01.026

DO - 10.1016/j.jid.2019.01.026

M3 - Comment/debate

C2 - 31010530

AN - SCOPUS:85064148849

SN - 0022-202X

VL - 139

SP - 995

EP - 996

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

IS - 5

ER -

Psoriasis Pathogenesis: Keratinocytes Are Back in the Spotlight

Abstract

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