scholarly journals A role for IL-25 and IL-33–driven type-2 innate lymphoid cells in atopic dermatitis

2013 ◽  
Vol 210 (13) ◽  
pp. 2939-2950 ◽  
Author(s):  
Maryam Salimi ◽  
Jillian L. Barlow ◽  
Sean P. Saunders ◽  
Luzheng Xue ◽  
Danuta Gutowska-Owsiak ◽  
...  

Type 2 innate lymphoid cells (ILC2s, nuocytes, NHC) require RORA and GATA3 for their development. We show that human ILC2s express skin homing receptors and infiltrate the skin after allergen challenge, where they produce the type 2 cytokines IL-5 and IL-13. Skin-derived ILC2s express the IL-33 receptor ST2, which is up-regulated during activation, and are enriched in lesional skin biopsies from atopic patients. Signaling via IL-33 induces type 2 cytokine and amphiregulin expression, and increases ILC2 migration. Furthermore, we demonstrate that E-cadherin ligation on human ILC2 dramatically inhibits IL-5 and IL-13 production. Interestingly, down-regulation of E-cadherin is characteristic of filaggrin insufficiency, a cardinal feature of atopic dermatitis (AD). ILC2 may contribute to increases in type 2 cytokine production in the absence of the suppressive E-cadherin ligation through this novel mechanism of barrier sensing. Using Rag1−/− and RORα-deficient mice, we confirm that ILC2s are present in mouse skin and promote AD-like inflammation. IL-25 and IL-33 are the predominant ILC2-inducing cytokines in this model. The presence of ILC2s in skin, and their production of type 2 cytokines in response to IL-33, identifies a role for ILC2s in the pathogenesis of cutaneous atopic disease.

2019 ◽  
Vol 143 (2) ◽  
pp. AB1
Author(s):  
Atsushi Kato ◽  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Kathryn E. Hulse ◽  
...  

2017 ◽  
Vol 139 (2) ◽  
pp. AB14
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Kathryn E. Hulse ◽  
...  

2013 ◽  
Vol 4 ◽  
Author(s):  
Salimi Maryam ◽  
Barlow Jillian ◽  
Saunders Sean ◽  
Xue Luzhend ◽  
Gutowska-Owsiak Danuta ◽  
...  

2018 ◽  
Vol 141 (3) ◽  
pp. 1147-1151.e8 ◽  
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Ava R. Weibman ◽  
...  

Diagnostics ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 808
Author(s):  
Yuichi Akama ◽  
Naoko Satoh-Takayama ◽  
Eiji Kawamoto ◽  
Atsushi Ito ◽  
Arong Gaowa ◽  
...  

Septic shock/severe sepsis is a deregulated host immune system response to infection that leads to life-threatening organ dysfunction. Lung inflammation as a form of acute lung injury (ALI) is often induced in septic shock. Whereas macrophages and neutrophils have been implicated as the principal immune cells regulating lung inflammation, group two innate lymphoid cells (ILC2s) have recently been identified as a new player regulating immune homeostasis. ILC2 is one of the three major ILC subsets (ILC1s, ILC2s, and ILC3s) comprised of newly identified innate immune cells. These cells are characterized by their ability to rapidly produce type 2 cytokines. ILC2s are predominant resident ILCs and, thereby, have the ability to respond to signals from damaged tissues. ILC2s regulate the immune response, and ILC2-derived type 2 cytokines may exert protective roles against sepsis-induced lung injury. This focused review not only provides readers with new insights into the signaling mechanisms by which ILC2s modulate sepsis-induced lung inflammation, but also proposes ILC2 as a novel therapeutic target for sepsis-induced ALI.


2020 ◽  
Vol 145 (1) ◽  
pp. 437-440.e8 ◽  
Author(s):  
Noriko Ogasawara ◽  
Julie A. Poposki ◽  
Aiko I. Klingler ◽  
Bruce K. Tan ◽  
Kathryn E. Hulse ◽  
...  

2020 ◽  
Vol 145 (2) ◽  
pp. AB193
Author(s):  
Janet Griffiths ◽  
Sriram Sridhar ◽  
Monica Gavala ◽  
Tuyet-Hang Pham ◽  
Yoichiro Ohne ◽  
...  

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