Treatment with a neutralising anti-rat interleukin-17 antibody after multiple-trauma reduces lung inflammation. 
It has been well recognised that a deficit of numbers and function of CD4(+)CD25(+)Foxp3(+) cells (Treg) is attributed to the development of autoimmune diseases and inflammatory diseases; additionally, IL-17-producing cells (Th17) have a pro-inflammatory role.  The balance between Th17 and Treg may be essential for maintaining immune homeostasis and has long been thought as one of the important factors in the development/prevention of autoimmune diseases and inflammatory diseases.  In our previous research, we explored that cytokines (IL-17) and the balance of Treg/Th17 had a significant relevance with tissue (lung) inflammation and injury in acute-phase after multiple-trauma.  To more verify whether an imbalance of Treg/Th17 is characteristic of rats suffering from multiple trauma.  Using IL-17 monoclonal antibody (IL-17mAb)-treated multiple-trauma rat, we tested the pathogenic role of IL-17 in the development of multiple-trauma.  Rat models were treated respectively with IL-17mAb or rat IgG 2A isotype control or phosphate-buffered solution after model was established.  Normal rats only received anaesthesia and cannulation were taken as sham.  Rats in each group were killed respectively at the end of 1h, 4h, 8h after injection.  Collected serum and lung samples for assessment dynamically of MPO, IL-17, IL-6, and TGF-β-mRNA, and cytokine (IL-17, IL-6, TGF-β) and lung tissue for pulmonary histological analysis.  Neutralisation of IL-17 with anti-IL-17 can decrease serum IL-17 level and the IL-17-mRNA transcript level in lung, and ameliorate tissue inflammatory, defer disease course.  Our data suggest that IL-17 is crucially involved in the pathogenesis of multiple-trauma in rat, IL-17 inhibition might ameliorate the lung inflammation in acute-phase after multiple-trauma.