The role of TSLP in IL-13-induced atopic march

Zhou Zhu; Min Hee Oh; Jinho Yu; Yong Jun Liu; Tao Zheng

doi:10.1038/srep00023

The role of TSLP in IL-13-induced atopic march

Zhou Zhu, Min Hee Oh, Jinho Yu, Yong Jun Liu, Tao Zheng

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

Abstract

Although atopic dermatitis (AD) is the initial step of the atopic march a progression from AD to asthma, the underlying mechanism remains unknown. Selective expression of IL-13 in the skin of mice caused an AD phenotype resembling human AD, and the disorder was associated with enhanced production of thymic stromal lymphopoietin (TSLP) in the AD skin with a systemic Th2 immunity. Here we show that IL-13 transgenic mice with AD had significantly enhanced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) when sensitized and challenged by allergen. In addition, the level of TSLP was significantly higher in acute AD than in chronic AD. Furthermore, elimination of TSLP signaling significantly diminished the allergic asthma responses, immune cell production of Th2 cytokines (IL-4, IL-13), and serum IgE. These studies indicate that IL-13 induces AD and atopic march via a TSLP dependent mechanism.

Original language	English (US)
Article number	23
Journal	Scientific reports
Volume	1
DOIs	https://doi.org/10.1038/srep00023
State	Published - 2011
Externally published	Yes

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@article{7120d8100c9a42698f3c44e1e722c251,

title = "The role of TSLP in IL-13-induced atopic march",

abstract = "Although atopic dermatitis (AD) is the initial step of the atopic march a progression from AD to asthma, the underlying mechanism remains unknown. Selective expression of IL-13 in the skin of mice caused an AD phenotype resembling human AD, and the disorder was associated with enhanced production of thymic stromal lymphopoietin (TSLP) in the AD skin with a systemic Th2 immunity. Here we show that IL-13 transgenic mice with AD had significantly enhanced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) when sensitized and challenged by allergen. In addition, the level of TSLP was significantly higher in acute AD than in chronic AD. Furthermore, elimination of TSLP signaling significantly diminished the allergic asthma responses, immune cell production of Th2 cytokines (IL-4, IL-13), and serum IgE. These studies indicate that IL-13 induces AD and atopic march via a TSLP dependent mechanism.",

author = "Zhou Zhu and Oh, {Min Hee} and Jinho Yu and Liu, {Yong Jun} and Tao Zheng",

note = "Funding Information: This work was supported by NIH grants R01AI075025 to T.Z. and R01HL079349 to Z.Z. The authors would like to thank Dr. Warren Leonard of NIH for providing the TSLP receptor deficient mice.",

year = "2011",

doi = "10.1038/srep00023",

language = "English (US)",

volume = "1",

journal = "Scientific reports",

issn = "2045-2322",

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T1 - The role of TSLP in IL-13-induced atopic march

AU - Zhu, Zhou

AU - Oh, Min Hee

AU - Yu, Jinho

AU - Liu, Yong Jun

AU - Zheng, Tao

N1 - Funding Information: This work was supported by NIH grants R01AI075025 to T.Z. and R01HL079349 to Z.Z. The authors would like to thank Dr. Warren Leonard of NIH for providing the TSLP receptor deficient mice.

PY - 2011

Y1 - 2011

N2 - Although atopic dermatitis (AD) is the initial step of the atopic march a progression from AD to asthma, the underlying mechanism remains unknown. Selective expression of IL-13 in the skin of mice caused an AD phenotype resembling human AD, and the disorder was associated with enhanced production of thymic stromal lymphopoietin (TSLP) in the AD skin with a systemic Th2 immunity. Here we show that IL-13 transgenic mice with AD had significantly enhanced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) when sensitized and challenged by allergen. In addition, the level of TSLP was significantly higher in acute AD than in chronic AD. Furthermore, elimination of TSLP signaling significantly diminished the allergic asthma responses, immune cell production of Th2 cytokines (IL-4, IL-13), and serum IgE. These studies indicate that IL-13 induces AD and atopic march via a TSLP dependent mechanism.

AB - Although atopic dermatitis (AD) is the initial step of the atopic march a progression from AD to asthma, the underlying mechanism remains unknown. Selective expression of IL-13 in the skin of mice caused an AD phenotype resembling human AD, and the disorder was associated with enhanced production of thymic stromal lymphopoietin (TSLP) in the AD skin with a systemic Th2 immunity. Here we show that IL-13 transgenic mice with AD had significantly enhanced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) when sensitized and challenged by allergen. In addition, the level of TSLP was significantly higher in acute AD than in chronic AD. Furthermore, elimination of TSLP signaling significantly diminished the allergic asthma responses, immune cell production of Th2 cytokines (IL-4, IL-13), and serum IgE. These studies indicate that IL-13 induces AD and atopic march via a TSLP dependent mechanism.

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The role of TSLP in IL-13-induced atopic march

Abstract

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