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Media type:
E-Article
Title:
Intraepithelial NK Cell-Derived IL-13 Induces Intestinal Pathology Associated with Nematode Infection
Contributor:
McDermott, Jacqueline R.;
Humphreys, Neil E.;
Forman, Simon P.;
Donaldson, Debra D.;
Grencis, Richard K.
imprint:
The American Association of Immunologists, 2005
Published in:The Journal of Immunology
Language:
English
DOI:
10.4049/jimmunol.175.5.3207
ISSN:
1550-6606;
0022-1767
Origination:
Footnote:
Description:
<jats:title>Abstract</jats:title>
<jats:p>IL-13 is a Th2-derived cytokine associated with pathological changes in asthma and ulcerative colitis. Moreover, it plays a major role in the control of gut nematode infection and associated immunopathology. The current paradigm is that these effects are due to T cell-derived IL-13. We show in this study that an innate source of IL-13, the intraepithelial NK cell, is responsible for the disruption of intestinal tissue architecture and induction of goblet cell hyperplasia that characterizes infection with the intestinal helminth Trichinella spiralis. IL-13 or IL-4Rα (but not IL-4) null mice failed to induce intestinal pathology. Unexpectedly, SCID and athymic mice developed the same pathology found in immunocompetent mice following infection. Moreover, immunodeficient mice expressed IL-13 in the intestine, and abnormal mucosal pathology was reduced by in vivo administration of a soluble IL-13 antagonist. IL-13 expression was induced in non-T intraepithelial CD3− NK cells. Epithelial cells expressed the IL-13 signaling receptor, IL-13Rα1, and after infection, IL-4Rα. Furthermore, the soluble IL-13 decoy receptor IL-13Rα2, which regulates IL-13 responses, was also induced upon infection. These data provide the first evidence that intestinal tissue restructuring during helminth infection is an innate event dependent on IL-13 production by NK cells resident in the epithelium of the intestine.</jats:p>