References
- Cha RH , YangSH, KimHS et al.: Genetic interactions between the donor and the recipient for susceptibility to acute rejection in kidney transplantation: polymorphisms of CCR5.Nephrol. Dial. Transplant.24(9) , 2919–2925 (2009).
- Prasad P , TiwariAK, KumarKM et al.: Association of TGFβ1, TNFα, CCR2 and CCR5 gene polymorphisms in Type-2 diabetes and renal insufficiency among Asian Indians.BMC Med. Genet.8 , 20 (2007).
- Rüster M , SperschneiderH, FünstückR, SteinG, GröneHJ: Differential expression of β-chemokines MCP-1 and RANTES and their receptors CCR1, CCR2, CCR5 in acute rejection and chronic allograft nephropathy of human renal allografts.Clin. Nephrol.61(1) , 30–39 (2004).
- Mengel M , JonigkD, MarwedelM et al.: Tubular chimerism occurs regularly in renal allografts and is not correlated to outcome.J. Am. Soc. Nephrol.15(4) , 978–986 (2004).
- Bastani S , ShermanW, SchnickelGT et al.: Chemokine receptor blockade with a synthetic nonpeptide compound attenuates cardiac allograft vasculopathy.Transplantation88(8) , 995–1001 (2009).
References
- Singh R , ManchandaPK, KesarwaniP, SrivastavaA, MittalRD: Influence of genetic polymorphisms in GSTM1, GSTM3, GSTT1 and GSTP1 on allograft outcome in renal transplant recipients.Clin. Transplant.23(4) , 490–498 (2009).
- Branten AJ , MulderTP, PetersWH, AssmannKJ, WetzelsJF: Urinary excretion of glutathione S transferases a and p in patients with proteinuria: reflection of the site of tubular injury.Nephron85(2) , 120–126 (2000).
- Yang Y , KaoMT, ChangCC et al.: Glutathione S-transferase T1 deletion is a risk factor for developing end-stage renal disease in diabetic patients.Int. J. Mol. Med.14(5) , 855–859 (2004).
- Aguilera I , Alvarez-MarquezA, GentilMA et al.: Anti-glutathione S-transferase T1 antibody-mediated rejection in C4d-positive renal allograft recipients.Nephrol. Dial. Transplant.23(7) , 2393–2398 (2008).
- Leonard MO , KieranNE, HowellK et al.: Reoxygenation-specific activation of the antioxidant transcription factor Nrf2 mediates cytoprotective gene expression in ischemia reperfusion injury.FASEB J.20(14) , 2624–2626 (2006).
References
- Le Meur Y , BüchlerM, ThierryA et al.: Individualized mycophenolate mofetil dosing based on drug exposure significantly improves patient outcomes after renal transplantation.Am. J. Transplant7(11) , 2496–503 (2007).
- van Gelder T , SilvaHT, de Fijter JW et al.: Comparing mycophenolate mofetil regimens for de novo renal transplant recipients: the fixed-dose concentration-controlled trial. Transplantation86(8) , 1043–1051 (2008).
- Gaston RS , KaplanB, ShahT et al.: Fixed- or controlled-dose mycophenolate mofetil with standard- or reduced-dose calcineurin inhibitors: the opticept trial.Am. J. Transplant9(7) , 1607–1619 (2009).
- van Schaik R , van Agteren M, de Fijter J et al.: UGT1A9-275T>A/-2152C>T polymorphisms correlate with low MPA exposure and acute rejection in MMF/tacrolimus-treated kidney transplant patients. Clin. Pharmacol. Ther.86(3) , 319–327 (2009).
- Kuypers DR , NaesensM, VermeireS, VanrenterghemY: The impact of uridine diphosphate-glucuronosyltransferase 1A9 (UGT1A9) gene promoter region single-nucleotide polymorphisms T-275A and C-2152T on early mycophenolic acid dose-interval exposure in de novo renal allograft recipients.Clin. Pharmacol. Ther.78(4) , 351–361 (2005).
References
- Piancatelli D , MaccaroneD, LiberatoreG et al.: HLA-G 14-bp insertion/deletion polymorphism in kidney transplant patients with metabolic complications.Transplant. Proc.41(4) , 1187–1188 (2009).
- Bahri R , HirschF, JosseA et al.: Soluble HLA-G inhibits cell cycle progression in human alloreactive T lymphocytes.J. Immunol.176(3) , 1331–1339 (2006).
- Naji A , DurrbachA, CarosellaED, Rouas-FreissN: Soluble HLA-G and HLA-G1 expressing antigen-presenting cells inhibit T-cell alloproliferation through ILT-2/ILT-4/FasL-mediated pathways.Hum. Immunol.68(4) , 233–239 (2007).
- Palikhe A , SinisaloJ, SeppänenM, ValtonenV, NieminenMS, LokkiML: Human MCH region harbors both susceptibility and protective haplotypes for coronary artery disease.Tissue Antigens69(1) , 47–55 (2007).