Chronic Rejection
Mostrando 25-36 de 97 artigos, teses e dissertações.
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25. PRECONDITIONING OF ORGAN DONORS WITH LOW LEVELS OF CARBON MONOXIDE REDUCES GRAFT IMMUNOGENICITY AND IMPROVES LONGTERM ALLOGRAFT FUNCTION
Background: Chronic rejection remains the major obstacle for successful transplantation, and to date there is no effective treatment. Events occurring prior to organ transplantation such as brain death, harvesting procedure, and ischemia-reperfusion injury lead to unspecific inflammatory damages danger signals - that increase graft immunogenicity and reduce
Publicado em: 2005
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26. The role of CD8+ T cells during allograft rejection
Organ transplantation can be considered as replacement therapy for patients with end-stage organ failure. The percent of one-year allograft survival has increased due, among other factors, to a better understanding of the rejection process and new immunosuppressive drugs. Immunosuppressive therapy used in transplantation prevents activation and proliferation
Brazilian Journal of Medical and Biological Research. Publicado em: 2002-11
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27. Cytokeratin immunostaining for detection of biliary epithelium: its use in counting bile ducts in cases of liver allograft rejection.
AIMS--To see how useful the application of a bile duct specific cytokeratin antibody (AE1) was in identifying and counting bile ducts in liver allograft biopsy specimens. METHODS--Eighteen liver biopsy specimens showing acute rejection and 17 biopsy specimens plus six hepatectomy specimens showing chronic rejection were studied. Serial sections were cut and
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28. Late blockade of T cell costimulation interrupts progression of experimental chronic allograft rejection.
Early blockade of T cell-costimulatory activation pathways prevents development of experimental chronic allograft rejection. Ongoing T cell recognition of alloantigen and activation may also play an important role in progression of chronic rejection, but definitive evidence is lacking. We used the fusion protein CTLA4Ig to block CD28-B7 T cell costimulation
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29. Blockade of T-cell costimulation prevents development of experimental chronic renal allograft rejection.
Blocking CD28-B7 T-cell costimulation by systemic administration of CTLA4Ig, a fusion protein which binds B7 molecules on the surface of antigen-presenting cells, prevents rejection and induces tolerance in experimental acute allograft rejection models. We tested the effect of CTLA4Ig therapy on the process of chronic renal allograft rejection using an estab
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30. Persistent allopeptide reactivity and epitope spreading in chronic rejection of organ allografts.
The role of the indirect allorecognition pathway in acute allograft rejection has been documented both in organ recipients and in experimental models. However, it is unknown whether self-restricted recognition of donor alloantigens also contributes to chronic allograft rejection. The aim of this study was to determine the relationship between allopeptide rea
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31. Sequential cytokine dynamics in chronic rejection of rat renal allografts: roles for cytokines RANTES and MCP-1.
Chronic rejection, the most important cause of long-term graft failure, is thought to result from both alloantigen-dependent and -independent factors. To examine these influences, cytokine dynamics were assessed by semiquantitative competitive reverse transcriptase-PCR and by immunohistology in an established rat model of chronic rejection lf renal allograft
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32. Targeting of the chemokine receptor CCR1 suppresses development of acute and chronic cardiac allograft rejection
Although mononuclear cell infiltration is a hallmark of cellular rejection of a vascularized allograft, efforts to inhibit rejection by blocking leukocyte-endothelial cell adhesion have proved largely unsuccessful, perhaps in part because of persistent generation of chemokines within rejecting grafts. We now provide, to our knowledge, the first evidence that
American Society for Clinical Investigation.
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33. Chronic cardiac rejection: identification of five upregulated genes in transplanted hearts by differential mRNA display.
Transplant arteriosclerosis, the major manifestation of chronic rejection, develops after allogeneic (Lewis to F344) but not syngeneic (Lewis to Lewis) rat cardiac transplantation. To identify transcriptionally regulated mediators associated with chronic cardiac rejection, we adapted the differential mRNA display technique for in vivo transplant specimens. G
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34. Critical roles for IL-4, IL-5, and eosinophils in chronic skin allograft rejection
C57BL/6 mice injected with the 145-2C11 anti-CD3 mAb and grafted with MHC class II disparate bm12 skin develop a chronic rejection characterized by interstitial dermal fibrosis, a marked eosinophil infiltrate, and an obliterative intimal vasculopathy. Because these changes occur in the absence of alloreactive antibodies, we examined the contribution of cytok
American Society for Clinical Investigation.
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35. Chronic cardiac rejection in the LEW to F344 rat model. Blockade of CD28-B7 costimulation by CTLA4Ig modulates T cell and macrophage activation and attenuates arteriosclerosis.
CTLA4Ig, a fusion protein that blocks CD28-B7 costimulation, was studied in a LEW to F344 rat model of chronic cardiac rejection. In rats treated with a single dose of CTLA4Ig (0.5 mg intraperitoneally) 2 d after transplantation, allografts survived significantly longer ( > 70 d in 64%) than in untreated controls or rats treated with control Ig (all rejected
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36. Tolerance and chronic rejection.
The most common cause of chronic allograft loss is an incompletely understood clinicopathological entity called chronic rejection (CR). Recent reports suggest an improvement in long-term renal allograft survival, although it is not clear from these data whether a true reduction of biopsy-proven CR has occurred. Although newer immunosuppressive medications ha