T helper 1, 2 and 17 cell subsets in renal transplant patients with delayed graft function

Antonia Loverre, Chiara Divella, Giuseppe Castellano, Tiziana Tataranni, Gianluigi Zaza, Michele Rossini, Pasquale Ditonno, Michele Battaglia, Silvano Palazzo, Margherita Gigante, Elena Ranieri, Francesco Paolo Schena, Giuseppe Grandaliano

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Ischemia-reperfusion injury (IRI) in kidney transplantation is the major cause of delayed graft function (DGF), an event associated with an increased risk of acute rejection. The aim of this study was to evaluate T helper (Th) cell phenotype in renal transplants with DGF. T-bet (Th1), GATA-3 (Th2) and IL-17 (Th17) protein expression was investigated in pretransplant biopsies, DGF and acute tubular damage (ATD) caused by calcineurin-inhibitor toxicity. Intracytofluorimetric analysis of IFN-Î, IL-4 and IL-17 was performed to analyze Th1, Th2 and Th17 responses in peripheral blood mononuclear cells of recipients with early graft function (EGF) and DGF, before (T0) and 24 h after transplantation (T24). In pretransplant biopsies, T-bet+, GATA-3 + and IL-17+ cells were barely detectable. In DGF, T-bet+ and IL-17+ cells were significantly increased compared with pretransplant and ATD. More than 90% of T-bet+ and less then 5% of IL-17+ cells were CD4+. GATA-3+ cells were increased to a lower extent. T-bet+/GATA-3+ cell ratio was significantly higher in DGF. Peripheral CD4+ IFN-Î/IL-4 ratio was significantly decreased in DGF, while CD4 +/IL-17+ cells did not differ between T0 and T24 in DGF. Our data suggest that DGF is characterized by a prevalent Th1 phenotype within the graft. This event might represent a link between DGF and acute rejection. Transplant International

Original languageEnglish
Pages (from-to)233-242
Number of pages10
JournalTransplant International
Volume24
Issue number3
DOIs
Publication statusPublished - Mar 2011

Fingerprint

Delayed Graft Function
Th17 Cells
Th2 Cells
Th1 Cells
Interleukin-17
Transplants
Kidney
Interleukin-4
Phenotype
Biopsy
Helper-Inducer T-Lymphocytes
Reperfusion Injury
Kidney Transplantation
Blood Cells
Transplantation

Keywords

  • adaptive immunity
  • delayed graft function
  • ischemia-reperfusion
  • kidney transplantation
  • T cells

ASJC Scopus subject areas

  • Transplantation

Cite this

Loverre, A., Divella, C., Castellano, G., Tataranni, T., Zaza, G., Rossini, M., ... Grandaliano, G. (2011). T helper 1, 2 and 17 cell subsets in renal transplant patients with delayed graft function. Transplant International, 24(3), 233-242. https://doi.org/10.1111/j.1432-2277.2010.01157.x

T helper 1, 2 and 17 cell subsets in renal transplant patients with delayed graft function. / Loverre, Antonia; Divella, Chiara; Castellano, Giuseppe; Tataranni, Tiziana; Zaza, Gianluigi; Rossini, Michele; Ditonno, Pasquale; Battaglia, Michele; Palazzo, Silvano; Gigante, Margherita; Ranieri, Elena; Schena, Francesco Paolo; Grandaliano, Giuseppe.

In: Transplant International, Vol. 24, No. 3, 03.2011, p. 233-242.

Research output: Contribution to journalArticle

Loverre, A, Divella, C, Castellano, G, Tataranni, T, Zaza, G, Rossini, M, Ditonno, P, Battaglia, M, Palazzo, S, Gigante, M, Ranieri, E, Schena, FP & Grandaliano, G 2011, 'T helper 1, 2 and 17 cell subsets in renal transplant patients with delayed graft function', Transplant International, vol. 24, no. 3, pp. 233-242. https://doi.org/10.1111/j.1432-2277.2010.01157.x
Loverre, Antonia ; Divella, Chiara ; Castellano, Giuseppe ; Tataranni, Tiziana ; Zaza, Gianluigi ; Rossini, Michele ; Ditonno, Pasquale ; Battaglia, Michele ; Palazzo, Silvano ; Gigante, Margherita ; Ranieri, Elena ; Schena, Francesco Paolo ; Grandaliano, Giuseppe. / T helper 1, 2 and 17 cell subsets in renal transplant patients with delayed graft function. In: Transplant International. 2011 ; Vol. 24, No. 3. pp. 233-242.
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abstract = "Ischemia-reperfusion injury (IRI) in kidney transplantation is the major cause of delayed graft function (DGF), an event associated with an increased risk of acute rejection. The aim of this study was to evaluate T helper (Th) cell phenotype in renal transplants with DGF. T-bet (Th1), GATA-3 (Th2) and IL-17 (Th17) protein expression was investigated in pretransplant biopsies, DGF and acute tubular damage (ATD) caused by calcineurin-inhibitor toxicity. Intracytofluorimetric analysis of IFN-{\^I}, IL-4 and IL-17 was performed to analyze Th1, Th2 and Th17 responses in peripheral blood mononuclear cells of recipients with early graft function (EGF) and DGF, before (T0) and 24 h after transplantation (T24). In pretransplant biopsies, T-bet+, GATA-3 + and IL-17+ cells were barely detectable. In DGF, T-bet+ and IL-17+ cells were significantly increased compared with pretransplant and ATD. More than 90{\%} of T-bet+ and less then 5{\%} of IL-17+ cells were CD4+. GATA-3+ cells were increased to a lower extent. T-bet+/GATA-3+ cell ratio was significantly higher in DGF. Peripheral CD4+ IFN-{\^I}/IL-4 ratio was significantly decreased in DGF, while CD4 +/IL-17+ cells did not differ between T0 and T24 in DGF. Our data suggest that DGF is characterized by a prevalent Th1 phenotype within the graft. This event might represent a link between DGF and acute rejection. Transplant International",
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