Background: Repeated attacks of acute rejection can result in chronic allograft dysfunction (CAD) which is the most prevalent cause of graft loss. T helper (Th) 17 cells, a newly identified subset of Th cells, are major mediators of inflammation-associated disease and have a reciprocal developmental relationship with the immunosuppressive regulatory T (Treg) cells, which actively restrain the inflammatory response. Th 17 has the exclusive ability to produce interleukin (IL)-17A. So, the present work was designed to study the balance between interleukin 17-secreting T helper cells and regulatory T cells after renal transplantation and their relation to graft function and survival.

Methods: Twenty patients with post renal transplantation and 20 healthy subjects were included in the study. The patients were further subdivided into two subgroups 10 patients each. Goup Ia, patients with stable renal allograft function and group Ib, patients with CAD. The Th cells, Th17 cells and Treg cells in fresh whole blood samples were identified as CD3⁺CD4⁺, CD4⁺IL17⁺ and CD4⁺CD25⁺FoxP3⁺ cells respectively using flow cytometry and expressed as percentages of total lymphocytes. Serum and urinary IL17A levels were measured using solid phase sandwich enzyme linked immunosorbant assay kit. Renal hemodynamics was evaluated by duplex Doppler ultrasonography and resistive and pulsatility indices (RI, PI) were calculated.

Results: Renal transplant recipients, especially patients with CAD, showed significant increases in the percentage of Th17 cells, total CD4⁺ Th cells, Th17/FoxP3⁺Treg ratio, serum and urinary IL17 levels and a significant decrease in the percentage of circulating FoxP3⁺Treg cells compared with healthy subjects (P< 0.01). The percentage of Th17 cells were positively correlated with serum and urinary IL17, Th17/FoxP3⁺Treg ratio, and inversely correlated with the percentage of circulating FoxP3⁺Treg cells (P< 0.01). The increased of RI and PI were positively correlated with renal function and cyclosporine trough level.

Conclusions: In renal transplant recipients the CD4⁺ Th cell phenotype is skewed toward the IL17 producing cells with the increase of serum IL 17. The imbalance between Th17 and Foxp3⁺ Treg cells plays an important role in graft dysfunction with deterioration of renal function.

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