Impact of donor and recipient cytokine genotypes on renal allograft outcome

Ligeiro, Dário; Sancho, M. R.; Papoila, Ana Luísa; Barradinhas, A.M; Almeida, Alan; Calão, S; Machado, Domingos; Nolasco, Fernando; Guerra, J.; Sampaio, M.; Trindade, Hélder

doi:10.1016/j.transproceed.2004.03.082

Cited by 23 publications

(19 citation statements)

References 9 publications

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“…Ligeiro et al. published the distribution of this polymorphism in a Portuguese population, which was also comparable to our results [25]. Larger population studies are yet to be conducted for this polymorphism.…”

Section: Discussionsupporting

confidence: 92%

The Relationship Between Interferon‐γ Gene Polymorphism and Acute Kidney Allograft Rejection

et al. 2011

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Cytokine gene polymorphisms have been associated with modified gene expression and cytokine production. Gamma interferon (IFN‐γ) plays an important role in the pathogenesis of kidney transplant rejection. This study evaluated the association between IFN‐γ gene polymorphisms and the history of acute allograft rejection in 53 adult first‐transplant recipients receiving cadaveric kidney grafts. They were followed up in a single centre until 2006, for a median time of 4 years after transplantation (1–22 years). IFN‐γ gene polymorphisms +874 T/A (rs2430561) were determined by polymerase chain reaction (PCR). T/T high IFN‐γ genotype was found in 12, intermediate T/A in 29 and low A/A in 12 patients. Twenty‐six acute kidney rejection episodes were evidenced in 20 patients, of which none occurred in the 12 patients with low IFN‐γ genotype A/A. Age, gender, number of HLA (human leukocyte antigen) mismatches, ABO blood groups, HLA, time after transplantation, creatinine clearance and immunosuppressive regimens were excluded as confounding factors associated with IFN‐γ genotype distribution between rejectors and non‐rejectors. IFN‐γ gene polymorphisms could be an important risk factor for acute kidney transplant rejection, whereas the low A/A IFN‐γ genotype could be protective against rejection.

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Section: Discussionsupporting

confidence: 92%

The Relationship Between Interferon‐γ Gene Polymorphism and Acute Kidney Allograft Rejection

et al. 2011

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“…Many factors have the potential to impact humoral alloimmunity after transplantation. Recipient and donor genetics impact the degree and specificity of alloantigen disparity (6-8), and influence the repertoire of cellular, cytokine and other factors which contribute to the resulting immune response (9, 10). The cells or organ to be transplanted determine the antigen load and expression of MHC and other molecules impacting the humoral immune responses evoked.…”

Section: Introductionmentioning

confidence: 99%

Critical Role of NKT Cells in Posttransplant Alloantibody Production

Zimmerer

Swamy

Sanghavi

et al. 2014

American Journal of Transplantation

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We previously reported that posttransplant alloantibody production in CD8-deficient hosts is IL-4+CD4+ T cell-dependent and IgG1 isotype-dominant. The current studies investigated the hypothesis that IL-4-producing NKT cells contribute to maximal alloantibody production. To investigate this, alloantibody levels were examined in CD8-deficient wild-type, CD1d KO and Jα18 KO transplant recipients. We found that the magnitude of IgG1 alloantibody production was critically dependent on the presence of type I NKT cells, which are activated by day 1 posttransplant. Unexpectedly, type I NKT cell contribution to enhanced IgG1 alloantibody levels was IFN-γ-dependent and IL-4-independent. Cognate interactions between Type I NKT and B cells alone do not stimulate alloantibody production. Instead, NKT cells appear to enhance maturation of IL-4+CD4+ T cells. To our knowledge, this is the first report to substantiate a critical role for type I NKT cells in enhancing in vivo antibody production in response to endogenous antigenic stimuli.

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“…Citation No association TNF -308G>A rs1800629 Sankaran et al, 1999;Pelletier et al, 2000;Poli et al, 2000;Hahn et al, 2001;Reviron et al, 2001;Wramner et al, 2004;Alakulppi et al, 2004;Grinyo et al, 2008;Pawlik et al, 2005;Tinckam et al, 2005;Lacha et al, 2005;Canossi et al, 2007;Coppo et al, 2007;Mendoza-Carrera et al, 2008;Nikolova et al, 2008;Pawlik et al, 2008;Grenda et al, 2009;La Manna et al, 2010;donor: Nikolova et al, 2008Hutchings et al, 2002Marshall et al, 2000;Cartwright et al, 2001;George et al, 2001;MullerSteinhardt et al, 2002;Weimer et al, 2003;McDaniel et al, 2003;Uboldi de Capei et al, 2004;Ligeiro et al, 2004;Dmitrienko et al, 2005;Gendzekhadze et al, 2006;Azarpira et al, 2006;Brabcova et al, 2007;Breulmann et al, 2007;Satoh et al, 2007;Rodrigo et al, 2007;Alakulppi et al, 2008;Azarpira et al, 2009;Kao et al, 2010;Jacobson et al, 2010;…”

Section: Gene Polymorphism Dbsnp Rs Number Citation Associationunclassified