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Lymphotoxin beta receptor signaling limits mucosal damage through driving IL-23 production by epithelial cells
- Source :
- Mucosal immunology
- Publication Year :
- 2014
-
Abstract
- The immune mechanisms regulating epithelial cell repair after injury remain poorly defined. We demonstrate here that lymphotoxin beta receptor (LTβR) signaling in intestinal epithelial cells promotes self-repair after mucosal damage. Using a conditional gene-targeted approach, we demonstrate that LTβR signaling in intestinal epithelial cells is essential for epithelial interleukin-23 (IL-23) production and protection against epithelial injury. We further show that epithelial-derived IL-23 promotes mucosal wound healing by inducing the IL-22-mediated proliferation and survival of epithelial cells and mucus production. Additionally, we identified CD4(-)CCR6(+)T-bet(-) RAR-related orphan receptor gamma t (RORγt)(+) lymphoid tissue inducer cells as the main producers of protective IL-22 after epithelial damage. Thus, our results reveal a novel role for LTβR signaling in epithelial cells in the regulation of intestinal epithelial cell homeostasis to limit mucosal damage.
- Subjects :
- Immunology
Gene Expression
C-C chemokine receptor type 6
Biology
Interleukin-23
Article
Epithelial Damage
Mice
RAR-related orphan receptor gamma
Lymphotoxin beta Receptor
T-Lymphocyte Subsets
medicine
Immunology and Allergy
Animals
Homeostasis
Intestinal Mucosa
Orphan receptor
Mice, Knockout
Wound Healing
Interleukins
Epithelial Cells
Colitis
Epithelium
Cell biology
Disease Models, Animal
medicine.anatomical_structure
Signal transduction
Wound healing
Lymphotoxin beta receptor
Signal Transduction
Subjects
Details
- ISSN :
- 19353456
- Volume :
- 8
- Issue :
- 2
- Database :
- OpenAIRE
- Journal :
- Mucosal immunology
- Accession number :
- edsair.doi.dedup.....53ba2f91abb37bf80db0c65ffa084217