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The mechanisms underlying maintenance of renal allografts in humans under minimal or conventional immunosuppression are poorly understood. There is evidence that CD4+ CD25+ regulatory T cells and clonal deletion, among other mechanisms of tolerance, could play a key role in clinical allograft survival. Twenty-four TCR-Vβ families were assessed in CD4+ CD25−, CD4+ CD25low and CD4+ CD25high T cells from patients with long-term renal allograft survival (LTS), patients exhibiting chronic rejection (ChrRx), patients on dialysis (Dial) and healthy controls (HC) by flow cytometry. LTS patients presented a higher variability in their TCR-Vβ repertoire, such decreased percentage of Vβ2+, Vβ8a+ and Vβ13+ in CD4+ CD25low and high compared with CD4+ CD25− subset and increased Vβ4 and Vβ7 families in CD4+ CD25high T cells exclusively. Additionally, LTS patients, particularly those that were not receiving calcineurin inhibitors (CNI), had increased percentages of CD4+ CD25high T cells when compared with Dial ( P < 0.05) and ChrRx ( P < 0.05) patients. Our results suggest that a differential expression of particular TCR-Vβ families and high levels of circulating CD4+ CD25high T cells in long-term surviving renal transplant patients could contribute to an active and specific state of immunologic suppression. However, the increase in this T cell subset with regulatory phenotype can be affected by CNI. [ABSTRACT FROM AUTHOR]