Unknown

Dataset Information

0

Cutting edge: regulation of intestinal inflammation and barrier function by IL-17C.


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 ?? 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.

SUBMITTER: Reynolds JM 

PROVIDER: S-EPMC3478486 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

altmetric image

Publications

Cutting edge: regulation of intestinal inflammation and barrier function by IL-17C.

Reynolds Joseph M JM   Martinez Gustavo J GJ   Nallaparaju Kalyan C KC   Chang Seon Hee SH   Wang Yi-Hong YH   Dong Chen C  

Journal of immunology (Baltimore, Md. : 1950) 20120928 9


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 w  ...[more]

Similar Datasets

| S-EPMC4684965 | biostudies-literature
| S-EPMC4707057 | biostudies-literature
| S-EPMC3718202 | biostudies-literature
| S-EPMC6275224 | biostudies-literature
| S-EPMC3577967 | biostudies-literature
| S-EPMC4308418 | biostudies-literature
| S-EPMC4592830 | biostudies-literature
| S-EPMC4278196 | biostudies-literature
| S-EPMC8556717 | biostudies-literature
| S-EPMC4947823 | biostudies-other