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Interleukin (IL)-23 mediates Toxoplasma gondii-induced immunopathology in the gut via matrixmetalloproteinase-2 and IL-22 but independent of IL-17

(2009) JOURNAL OF EXPERIMENTAL MEDICINE. 206(13). p.3047-3059
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Abstract
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.
Keywords
ULCERATIVE-COLITIS, INTESTINAL INFLAMMATION, INTERFERON-GAMMA, NKP46(+) CELLS, INFLAMMATORY-BOWEL-DISEASE, T-CELL, TH17 CELLS, MURINE MODEL, ORAL INFECTION, MATRIX METALLOPROTEINASES

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Chicago
Munoz, Melba, Markus M Heimesaat, Kerstin Danker, Daniela Struck, Uwe Lohmann, Rita Plickert, Stefan Bereswill, et al. 2009. “Interleukin (IL)-23 Mediates Toxoplasma Gondii-induced Immunopathology in the Gut via Matrixmetalloproteinase-2 and IL-22 but Independent of IL-17.” Journal of Experimental Medicine 206 (13): 3047–3059.
APA
Munoz, M., Heimesaat, M. M., Danker, K., Struck, D., Lohmann, U., Plickert, R., Bereswill, S., et al. (2009). Interleukin (IL)-23 mediates Toxoplasma gondii-induced immunopathology in the gut via matrixmetalloproteinase-2 and IL-22 but independent of IL-17. JOURNAL OF EXPERIMENTAL MEDICINE, 206(13), 3047–3059.
Vancouver
1.
Munoz M, Heimesaat MM, Danker K, Struck D, Lohmann U, Plickert R, et al. Interleukin (IL)-23 mediates Toxoplasma gondii-induced immunopathology in the gut via matrixmetalloproteinase-2 and IL-22 but independent of IL-17. JOURNAL OF EXPERIMENTAL MEDICINE. 2009;206(13):3047–59.
MLA
Munoz, Melba et al. “Interleukin (IL)-23 Mediates Toxoplasma Gondii-induced Immunopathology in the Gut via Matrixmetalloproteinase-2 and IL-22 but Independent of IL-17.” JOURNAL OF EXPERIMENTAL MEDICINE 206.13 (2009): 3047–3059. Print.
@article{822840,
  abstract     = {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.},
  author       = {Munoz, Melba and Heimesaat, Markus M and Danker, Kerstin and Struck, Daniela and Lohmann, Uwe and Plickert, Rita and Bereswill, Stefan and Fischer, Andre and Dunay, Ildiko Rita and Wolk, Kerstin and Loddenkemper, Christoph and Krell, Hans-Willi and Libert, Claude and Lund, Leif R and Frey, Oliver and Holscher, Christoph and Iwakura, Yoichiro and Ghilardi, Nico and Ouyang, Wen-Jun and Kamradt, Thomas and Sabat, Robert and Liesenfeld, Oliver},
  issn         = {0022-1007},
  journal      = {JOURNAL OF EXPERIMENTAL MEDICINE},
  language     = {eng},
  number       = {13},
  pages        = {3047--3059},
  title        = {Interleukin (IL)-23 mediates Toxoplasma gondii-induced immunopathology in the gut via matrixmetalloproteinase-2 and IL-22 but independent of IL-17},
  url          = {http://dx.doi.org/10.1084/jem.20090900},
  volume       = {206},
  year         = {2009},
}

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