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Background   CD 4+ T helper (Th) cells, including Th1, Th2, and Th17 cells, play critical roles in angiotensin  II –induced hypertension. Th22 cells, a novel subset of Th cells, take part in cardiovascular diseases by producing  IL ‐22 (interleukin 22). This study aimed to investigate whether  IL ‐22 is involved in hypertension.    Methods and Results  Th22 cells and  IL ‐22 levels were detected in angiotensin  II –infused mice, and the results showed that Th22 cells and  IL ‐22 levels significantly increased. To determine the effect of Th22/ IL ‐22 on blood pressure regulation, angiotensin  II –infused mice were treated with recombinant mouse  IL ‐22, an anti– IL ‐22 neutralizing monoclonal antibody, or control. Treatment with recombinant  IL ‐22 resulted in increased blood pressure, amplified inflammatory responses, and aggravated endothelial dysfunction, whereas the anti– IL ‐22 neutralizing monoclonal antibody decreased blood pressure, reduced inflammatory responses, and attenuated endothelial dysfunction. To determine whether the  STAT 3 (signal transducer and activator of transcription 3) pathway mediates the effect of  IL ‐22 on blood pressure regulation, the special  STAT 3 pathway inhibitor S31‐201 was administered to mice treated with recombinant  IL ‐22. S31‐201 treatment significantly ameliorated the  IL ‐22 effects of increased blood pressure and endothelial dysfunction. In addition, serum  IL ‐22 levels were significantly increased in hypertensive patients compared with healthy persons. Correlation analysis showed a positive correlation between  IL ‐22 levels and blood pressure.    Conclusions   IL ‐22 amplifies the inflammatory response, induces endothelial dysfunction and promotes blood pressure elevation in angiotensin  II –induced hypertensive mice. The  STAT 3 pathway mediates the effect of  IL ‐22 on hypertension. Blocking  IL ‐22 may be a novel therapeutic strategy to prevent and treat hypertension.

Interleukin 22 Promotes Blood Pressure Elevation and Endothelial Dysfunction in Angiotensin II –Treated Mice