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T cell receptor beta chain (TCR-Vbeta) repertoire of circulating CD4(+) CD25(-), CD4(+) CD25(low) and CD4(+) CD25(high) T cells in patients with long-term renal allograft survival

T cell receptor beta chain (TCR-Vbeta) repertoire of circulating CD4(+) CD25(-), CD4(+) CD25(low) and CD4(+) CD25(high) T cells in patients with long-term renal allograft survival

Transplant International 23(1): 54-63

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-Vbeta families were assessed in CD4(+) CD25(-), CD4(+) CD25(low) and CD4(+) CD25(high) 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-Vbeta repertoire, such decreased percentage of Vbeta2(+), Vbeta8a(+) and Vbeta13(+) in CD4(+) CD25(low) and (high) compared with CD4(+) CD25(-) subset and increased Vbeta4 and Vbeta7 families in CD4(+) CD25(high) T cells exclusively. Additionally, LTS patients, particularly those that were not receiving calcineurin inhibitors (CNI), had increased percentages of CD4(+) CD25(high) 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-Vbeta families and high levels of circulating CD4(+) CD25(high) 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.

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Accession: 056098095

Download citation: RISBibTeXText

PMID: 19694999

DOI: 10.1111/j.1432-2277.2009.00946.x

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