Disease relevance of Transplantation, Homologous

• A randomized, placebo-controlled trial of oral acyclovir for the prevention of cytomegalovirus disease in recipients of renal allografts [1].
• Among the patients with stable allograft function and serum creatinine concentrations below 265 mumol per liter, hyperuricemia was more common in the cyclosporine group than in the azathioprine group (84 percent vs. 30 percent; P = 0.0001) [2].
• Moreover, in mouse models of atheroma formation or allogeneic transplantation, the serological neutralization or genetic absence of IFN-gamma markedly reduces the extent of intimal expansion [3].
• The striatal allografts also reduce the occurrence of dystonia, a major abnormal movement associated with HD [4].
• The multichain interleukin 2 receptor. A target for immunotherapy in lymphoma, autoimmune disorders, and organ allografts [clinical reference] [5].

Psychiatry related information on Transplantation, Homologous

• The identified human antibodies to CCR5 define an alloantigen that may cause allograft rejection in a mismatch situation even in individuals with no history of blood transfusions or i.v. drug abuse [6].
• One patient sustained acute allograft rejection as a result of patient noncompliance, and one patient on a seemingly appropriate CsA/Aza/Pred dose responded initially to steroid pulse antirejection therapy; however, renal function again worsened [7].

High impact information on Transplantation, Homologous

• The underlying science and the prospects for inducing long-lived antigen-specific tolerance in a model of allograft tolerance through CD154 blockade are presented and discussed [8].
• New forms of therapy directed at IL-2 and IL-15 receptors may be effective against certain neoplastic diseases and autoimmune disorders and in the prevention of allograft rejection [9].
• Rejection of transplanted tissue allografts results from T-cell recognition of histocompatibility antigens expressed by cells of the donor graft [10].
• Messenger RNA (mRNA) encoding the cytotoxic proteins perforin and granzyme B and a constitutively expressed cyclophilin B gene were measured with the use of a competitive, quantitative polymerase chain reaction, and the level of expression was correlated with allograft status [11].
• MPA is a potent IMPDH inhibitor and the active metabolite of an immunosuppressive drug recently approved for the treatment of allograft rejection [12].

Chemical compound and disease context of Transplantation, Homologous

• Immunity to Epstein-Barr virus in cyclosporin A-treated renal allograft recipients [13].
• Hematologic toxicity occurred when trimethoprim-sulfamethoxazole was given for prolonged periods to renal allograft subjects also treated with azathioprine [14].
• These results suggest that factors other than cyclosporine A are responsible for the interstitial fibrosis observed in cardiac allografts [15].
• Between December 1997 and March 2000, 40 patients, aged 21 to 67 years (median 51), with hematologic malignancies underwent nonmyeloablative allografts after either 2 Gy total body irradiation alone (n = 30) or 2 Gy total body irradiation preceded by fludarabine 30 mg/m(2)/d on days -4, -3, and -2 (n = 10) [16].
• Determination of neopterin [D-erythro-6-(1',2',3'-trihydroxypropyl)pterin] in body fluids is a powerful diagnostic tool in a variety of diseases in which activation of cellular immune mechanisms is involved, such as certain malignancies, allograft rejection, and autoimmune and infectious diseases [17].

Biological context of Transplantation, Homologous

• Gene expression analyses showed that there is a substantial decrease in the genes encoding RANKL and VEGF during allograft healing [18].
• The results suggest that disparities in major histocompatibility complex antigens of class I (H-2K and H-2D) alone are capable of eliciting islet allograft rejection, and that lack of a stimulus from class II (I-region) alloantigens does not ensure permanent islet allograft survival [19].
• Stability of allograft glomerular filtration rate (GFR) in each patient was assessed by calculating the slope of a plot of the reciprocal of the serum creatinine concentration vs time [20].
• In contrast, allografts in iNOS(-/-) recipients exhibited reductions in local expression of proinflammatory chemokines and cytokines, graft T cell recruitment and apoptosis, and luminal obliteration (29 +/- 2%, P < 0.05 vs. WT allografts) [21].
• DA rats grafted with major histocompatibility complex-incompatible PVG heart grafts and treated with cyclosporine (CY) for 10 d do not reject their grafts, and develop a state of specific unresponsiveness toward PVG allografts [22].

Anatomical context of Transplantation, Homologous

• Coronary artery disease developed during follow-up in 31 of 40 allografts (78 percent) with depletion of t-PA, but the disease developed in only 9 of the 38 allografts (24 percent) with normal t-PA levels (P < 0.001) [23].
• In addition to their clinical importance in the prevention of allograft rejection, cyclosporin A and FK-506 represent important reagents for the study of the molecular mechanisms of lymphocyte activation [24].
• NK cells promote islet allograft tolerance via a perforin-dependent mechanism [25].
• Immunological unresponsiveness to allografts can be achieved by pretreating recipients with cells (whole blood, erythrocytes, lymphocytes) expressing donor-specific histocompatibility antigens [26].
• An indefinite survival of cardiac allografts between fully incompatible mice strains was observed when monoclonal antibodies (MAbs) to intercellular adhesion molecule-1 (ICAM-1) and leukocyte function-associated antigen-1 (LFA-1) were simultaneously administered after the transplantation for 6 days [27].

Associations of Transplantation, Homologous with chemical compounds

• Update for the Canadian multicentre trial of cyclosporine in renal allografts [28].
• We prospectively studied the magnitude, distribution, and mechanism of bone loss in 20 adults who received renal allografts from living related donors, who had good renal function, and who were treated with azathioprine, cyclosporine, and low doses of prednisone [29].
• It is more than thirty years since Billingham and Medawar showed that adrenocorticotrophic hormone (ACTH) and cortisol can prolong the survival of skin allografts [30].
• In vivo, administration of azodicarbonamide into mice blunted their response to polyclonal T-cell activation induced by the injection of monoclonal antibody against CD3 and resulted in delayed rejection of skin allografts [31].
• In addition, the calculated creatinine clearance at 1 year had an adjusted rate ratio (RR) for allograft failure per 10 mL/min (0.17 mL/s) of 0.74 (95% confidence interval [CI], 0.62-0.88) [32].

Gene context of Transplantation, Homologous

• Thus, the FasL signal provided site- and immune-specific protection of islet allografts [33].
• Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability [34].
• Requirement of the chemokine receptor CXCR3 for acute allograft rejection [35].
• However, though allografts from IP-10(+/+) mice were rejected by day 7, hearts from IP-10(-/-) mice survived long term [36].
• Recruitment of Foxp3+ T regulatory cells mediating allograft tolerance depends on the CCR4 chemokine receptor [37].

Analytical, diagnostic and therapeutic context of Transplantation, Homologous

• Cyclosporine provides adequate immunosuppression for patients with renal allografts [38].
• Effect of HLA typing and transfusions on cyclosporine-treated renal allograft recipients [39].
• In conclusion, we find that RANKL and VEGF are necessary and sufficient for efficient autograft remodeling and can be transferred using rAAV to revitalize structural allografts [18].
• Within 24 h (and even within 4 h of culture), LC in epidermal sheets from allografts, isografts, and explants dramatically increased in size and expression of major histocompatibility complex class II molecules, and their numbers were markedly decreased [40].
• Real-time polymerase chain reaction showed that intragraft Foxp3 levels in tolerized recipients were approximately 100-fold higher than rejecting allografts or allografts associated with other therapies inducing prolonged survival but not tolerance [37].

References