NOD2 drives early IL-33–dependent expansion of group 2 innate lymphoid cells during Crohn’s disease–like ileitis
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Title
NOD2 drives early IL-33–dependent expansion of group 2 innate lymphoid cells during Crohn’s disease–like ileitis
Authors
Keywords
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Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 131, Issue 5, Pages -
Publisher
American Society for Clinical Investigation
Online
2021-01-15
DOI
10.1172/jci140624
References
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Related references
Note: Only part of the references are listed.- Innate lymphoid cells support regulatory T cells in the intestine through interleukin-2
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- Innate Lymphoid Cells in Intestinal Inflammation
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- IL-33 Drives Eosinophil Infiltration and Pathogenic Type 2 Helper T-Cell Immune Responses Leading to Chronic Experimental Ileitis
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- IL-12 drives functional plasticity of human group 2 innate lymphoid cells
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- Genetic deletion of the bacterial sensor NOD2 improves murine Crohn’s disease-like ileitis independent of functional dysbiosis
- (2016) D Corridoni et al. Mucosal Immunology
- Interleukin-12 and -23 Control Plasticity of CD127+ Group 1 and Group 3 Innate Lymphoid Cells in the Intestinal Lamina Propria
- (2015) Jochem H. Bernink et al. IMMUNITY
- Stereomicroscopic 3D-pattern profiling of murine and human intestinal inflammation reveals unique structural phenotypes
- (2015) Alex Rodriguez-Palacios et al. Nature Communications
- Dysregulated NOD2 predisposes SAMP1/YitFc mice to chronic intestinal inflammation
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- Mutated Major Histocompatibility Complex Class II Transactivator Up-regulates Interleukin-33-dependent Differentiation of Th2 Subset through Nod2 Binding for NLR (NOD-like Receptor) Signaling Initiation
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- SAMP1/YitFc mouse strain: A spontaneous model of Crohnʼs disease-like ileitis
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- Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity
- (2010) Daniel R. Neill et al. NATURE
- Epithelial-derived IL-33 and its receptor ST2 are dysregulated in ulcerative colitis and in experimental Th1/Th2 driven enteritis
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