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Soluble Immune Molecules Cause Acute Kidney Inflammation in Mice

ScienceDaily (Dec. 14, 2009) — 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.

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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. 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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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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