Abstract
A robust inflammatory response involving tumor necrosis factor-α (TNFα) is induced during cisplatin nephrotoxicity. Using chimeric models, Reeves and colleagues now demonstrate that resident kidney cells, rather than infiltrating immune cells, are the major producers of TNF-α. Blockade of TNFα attenuates inflammation and associated kidney injury.
Original language | English (US) |
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Pages (from-to) | 5-7 |
Number of pages | 3 |
Journal | Kidney International |
Volume | 72 |
Issue number | 1 |
DOIs |
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State | Published - Jul 2007 |
ASJC Scopus subject areas
- Nephrology