Lymphocyte specific deletion of IKK2 or NEMO mediates increase of intrarenal Th17 cells and accelerates renal damage in ischemia reperfusion injury mouse model.

In conclusion, although systemic IKK2 inhibition improved kidney function, lymphocyte-specific deletion of IKK2 or NEMO aggravated kidney injury after IRI, and in both conditions, the percentage of Th17 cells was increased. Our findings demonstrate the critical role of the NF-κB pathway in Th17 activation, which advises caution when using systemic IKK2 inhibitors in patients with kidney injury as they might impair the T cell response and aggravate renal disease.
PMID: 27582100 [PubMed - as supplied by publisher]

Source: Am J Physiol Renal P... - August 30, 2016 Category: Urology & Nephrology Authors: Guo L, Lee HH, Noriega ML, Paust HJ, Zahner G, Thaiss F Tags: Am J Physiol Renal Physiol Source Type: research