Abstract
Th17 cells are known to have potent proinflammatory functions in human inflammatory and autoimmune diseases. Therefore, it is tempting to speculate that Th17 cells and their effector cytokines are significant in the inflammatory response after organ transplantation. These Th17 cell mediated immune responses are suppressed by FOXP3+ regulatory T cells. Here, we studied the involvement of IL-17 and FOXP3 in the rejection process after clinical heart transplantation. The traditional players in acute rejection IL-2 and IFN-γ were measured as a control.
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