Effect of the TNF-α–promoter polymorphism on cardiac allograft rejection

Genetic Polymorphism in Platelet-derived Growth Factor and Vascular Endothelial Growth Factor Are Significantly Associated With Cardiac Allograft Vasculopathy

“…Our results did not corroborate the findings in studies by Turner et al, 27 Azzawi et al 28 and Awad et al, 29 who reported a significant association between recipients phenotyped as high producers of TNF-␣ and a high risk to develop acute cellular rejection. Similar results were recently reported by Bedi et al 30 In addition, we did not substantiate the association between acute cellular rejection and low IL-10 production phenotype, as reported by Turner et al 27 and Awad et al 29 Although Plaza et al 31 showed an association between low IL-10 genotype and Quilty-type EMB, Bijlsma et al 32 reported no significant association between IL-10 and acute transplant rejection. Similar data were reported by other groups concluding that there is no association between acute allograft rejection and multiple cytokines, including TNF-␣, TGF-␤, IFN-␥, IL-6 and IL-10.…”

Pharmacogenomics and lung transplantation: clinical implications

“…41,43,44 Some heart transplant studies do not support this observation, but these discrepancies may result from differences between rejection criteria (ISHLT grade X2 compared to X3A) or a smaller population size with limited statistical power. [48][49][50] In lung transplant recipients, we did not observe an increase in risk of refractory rejection associated with TNF-a high genotype. 33 In liver transplant recipients, the TNF-a high genotype was associated with acute rejection in some studies [51][52][53] but not in others.…”

Inhibition of Tumor Necrosis Factor-α Attenuates Myocardial Remodeling in Rat Cardiac Allografts

“…14 However, increased TNF-␣ production was not associated with increased risk of rejection in adult cardiac transplant recipients. 15 Studies have indicated that TNF-␣ regulates the platelet-derived growth factor (PDGF)-A/PDGF-R␣ activation pathway in rat cardiac allograft arteriosclerosis. 16 To test this hypothesis, rats with heterotopic cardiac allografts received TNF-␣ antagonist in the form of recombinant human soluble TNF receptor p80/IgG1 Fc fusion protein (rhu TNF-R2:Fc).…”