Soluble immune molecules cause acute kidney inflammation in mice
- Date:
- December 14, 2009
- Source:
- Journal of Clinical Investigation
- Summary:
- Immune molecules known as cytokines are effectors of immune cell function. The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have been linked to autoimmune diseases (i.e, diseases in which the immune system turns on the body). Researchers have now determined that these cytokine pathways also contribute to inflammation in a mouse model of acute kidney injury.
- Share:
Immune molecules known as cytokines are effectors of immune cell function. The IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways have been linked to autoimmune diseases (i.e, diseases in which the immune system turns on the body).
A team of researchers, led by Li Li, at the University of Virginia, Charlottesville, has now determined that these cytokine pathways also contribute to inflammation in a mouse model of acute kidney injury.
Specifically, they find that the IL-23/IL-17 pathway works upstream of the IL-12/IFN-gamma pathway, as IL-17A production by immune cells known as neutrophils was required for activation of the IL-12/IFN-gamma pathway.
In addition, as the inflammation underlying kidney injury in this model was caused by blood flow returning to the kidney following a period in which the kidney was deprived of blood flow (an event known as reperfusion) and reperfusion injury has a role in brain and heart damage caused by stroke and heart attack, respectively, the authors suggest that the IL-23/IL-17 and IL-12/IFN-gamma cytokine pathways might contribute to reperfusion injury in other organs.
The research is reported in the Journal of Clinical Investigation.
Story Source:
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
Journal Reference:
- li Li, Liping Huang, Amy L. Vergis, Hong Ye, Amandeep Bajwa, Vivek Narayan, Robert M. Strieter, Diane L. Rosin, and Mark D. Okusa. IL-17 produced by neutrophils regulates IFN-γ–mediated neutrophil migration in mouse kidney ischemia-reperfusion injury. Journal of Clinical Investigation, 2009; DOI: 10.1172/JCI38702
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