Abstract
In the IL-17 family of cytokines, much is known about the sources and functions of IL-17, IL-17F, and IL-25 in the host defense against infection and in inflammatory diseases; however, the physiological function of IL-17C remains poorly understood. Using mice deficient in IL-17C, we demonstrate that this cytokine is crucial for the regulation of an acute experimental colitis elicited by dextran sulfate sodium. In this model, mice lacking IL-17C exhibited exacerbated disease that was associated with increased IL-17 expression by γδ T cells and Th17 cells. Moreover, IL-17C directly regulated the expression of the tight junction molecule occludin by colonic epithelial cells. Thus, our data suggest that IL-17C plays a critical role in maintaining mucosal barrier integrity.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Cell Line
-
Colitis / genetics
-
Colitis / immunology*
-
Colitis / pathology*
-
Colon / cytology
-
Colon / immunology
-
Colon / pathology
-
Dextran Sulfate / toxicity
-
Disease Models, Animal
-
Epithelium / immunology
-
Epithelium / metabolism
-
Epithelium / pathology
-
Genetic Predisposition to Disease
-
Inflammation Mediators / metabolism
-
Inflammation Mediators / physiology*
-
Interleukin-17 / biosynthesis
-
Interleukin-17 / deficiency
-
Interleukin-17 / physiology*
-
Intestinal Mucosa / immunology*
-
Intestinal Mucosa / metabolism
-
Intestinal Mucosa / pathology*
-
Male
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
Substances
-
Il17c protein, mouse
-
Inflammation Mediators
-
Interleukin-17
-
Dextran Sulfate