Interleukin-22 promotes intestinal-stem-cell-mediated epithelial regeneration View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

Caroline A. Lindemans, Marco Calafiore, Anna M. Mertelsmann, Margaret H. O’Connor, Jarrod A. Dudakov, Robert R. Jenq, Enrico Velardi, Lauren F. Young, Odette M. Smith, Gillian Lawrence, Juliet A. Ivanov, Ya-Yuan Fu, Shuichiro Takashima, Guoqiang Hua, Maria L. Martin, Kevin P. O’Rourke, Yuan-Hung Lo, Michal Mokry, Monica Romera-Hernandez, Tom Cupedo, Lukas E. Dow, Edward E. Nieuwenhuis, Noah F. Shroyer, Chen Liu, Richard Kolesnick, Marcel R. M. van den Brink, Alan M. Hanash

ABSTRACT

Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. The intestinal stem cell (ISC) niche provides Wnt, Notch and epidermal growth factor (EGF) signals supporting Lgr5(+) crypt base columnar ISCs for normal epithelial maintenance. However, little is known about the regulation of the ISC compartment after tissue damage. Using ex vivo organoid cultures, here we show that innate lymphoid cells (ILCs), potent producers of interleukin-22 (IL-22) after intestinal injury, increase the growth of mouse small intestine organoids in an IL-22-dependent fashion. Recombinant IL-22 directly targeted ISCs, augmenting the growth of both mouse and human intestinal organoids, increasing proliferation and promoting ISC expansion. IL-22 induced STAT3 phosphorylation in Lgr5(+) ISCs, and STAT3 was crucial for both organoid formation and IL-22-mediated regeneration. Treatment with IL-22 in vivo after mouse allogeneic bone marrow transplantation enhanced the recovery of ISCs, increased epithelial regeneration and reduced intestinal pathology and mortality from graft-versus-host disease. ATOH1-deficient organoid culture demonstrated that IL-22 induced epithelial regeneration independently of the Paneth cell niche. Our findings reveal a fundamental mechanism by which the immune system is able to support the intestinal epithelium, activating ISCs to promote regeneration. More... »

PAGES

560

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature16460

DOI

http://dx.doi.org/10.1038/nature16460

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1006486442

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26649819


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494 Department of Medicine, Weill Cornell Medicine, New York, New York 10021, USA
495 rdf:type schema:Organization
496 https://www.grid.ac/institutes/grid.5645.2 schema:alternateName Erasmus University Medical Center
497 schema:name Department of Hematology, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands
498 rdf:type schema:Organization
499 https://www.grid.ac/institutes/grid.7692.a schema:alternateName University Medical Center Utrecht
500 schema:name Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
501 Department of Pediatrics, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands
502 rdf:type schema:Organization
 




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