Epithelial IL-23R Signaling Licenses Protective IL-22 Responses in Intestinal Inflammation
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- 作者：Konrad Aden1 ; 2 ; Ateequr Rehman1 ; Maren Falk-Paulsen1 ; Thomas Secher3 ; Jan Kuiper1 ; Florian Tran1 ; Steffen Pfeuffer1 ; Raheleh Sheibani-Tezerji1 ; Alexandra Breuer1 ; Anne Luzius1 ; Marlene Jentzsch1 ; Robert Hä ; sler1 ; Susanne Billmann-Born1 ; Olga Will1 ; Simone Lipinski1 ; Richa Bharti1 ; Timon Adolph4 ; Juan L. Iovanna5 ; Sarah L. Kempster4 ; Richard S. Blumberg6 ; Stefan Schreiber1 ; 2 ; Burkhard Becher7 ; Mathias Chamaillard8 ; Arthur Kaser4 ; Philip Rosenstiel1 ; 9 ; p.rosenstiel@mucosa.de" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cell Reports
- 出版年：2016
- 出版时间：23 August 2016
- 年：2016
- 卷：16
- 期：8
- 页码：2208-2218
- 全文大小：3490 K
文摘
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IL-23R transduces signals into the intestinal epithelium
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Il23RΔIEC mice are susceptible to DSS colitis and have a disturbed gut microflora
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Epithelial IL-23R is required for optimal secretion of the c-type lectin Reg3b
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The c-type lectin Reg3b promotes recruitment of IL-22-producing cells as an alarmin
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Systemic substitution of Reg3b rescues the gut barrier defect of Il23RΔIEC mice