In:
Journal of Experimental Medicine, Rockefeller University Press, Vol. 206, No. 13 ( 2009-12-21), p. 3047-3059
Kurzfassung:
Peroral infection with Toxoplasma gondii leads to the development of small intestinal inflammation dependent on Th1 cytokines. The role of Th17 cells in ileitis is unknown. We report interleukin (IL)-23–mediated gelatinase A (matrixmetalloproteinase [MMP]-2) up-regulation in the ileum of infected mice. MMP-2 deficiency as well as therapeutic or prophylactic selective gelatinase blockage protected mice from the development of T. gondii–induced immunopathology. Moreover, IL-23–dependent up-regulation of IL-22 was essential for the development of ileitis, whereas IL-17 was down-regulated and dispensable. CD4+ T cells were the main source of IL-22 in the small intestinal lamina propria. Thus, IL-23 regulates small intestinal inflammation via IL-22 but independent of IL-17. Gelatinases may be useful targets for treatment of intestinal inflammation.
Materialart:
Online-Ressource
ISSN:
1540-9538
,
0022-1007
DOI:
10.1084/jem.20090900
Sprache:
Englisch
Verlag:
Rockefeller University Press
Publikationsdatum:
2009
ZDB Id:
1477240-1
