The role of the B7 costimulatory pathway in experimental cold ischemia/reperfusion injury.

Takada, Moriatsu; Chandraker, Anil; Nadeau, Kari; Sayegh, Mohamed H.; Tilney, Nicholas L.

doi:10.1172/jci119632

Cited by 212 publications

(136 citation statements)

References 34 publications

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“…Experimentally, kidneys and hearts transplanted from BD animals show accelerated acute rejection in comparison to grafts from living donors (2). This is thought to be triggered by an increased release of proinflammatory cytokines (2,5,31), an up-regulation of major histocompatibility complex (MHC/HLA class I and II) antigens and co-stimulating B7 in peripheral organs (5,32).…”

Section: Discussionmentioning

confidence: 99%

Brain Death Impairs Pancreatic Microcirculation

Obermaier

Dobschuetz

Keck

et al. 2004

American Journal of Transplantation

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Brain death (BD) influences the quality of donor grafts in transplantation. To evaluate the impact of BD on pancreas grafts, we investigated the influence of BD on the microcirculation and histology of the pancreas in a rat model of explosive BD. A group of Wistar rats (n = = 7), rendered brain dead by inflating an intracranially inserted Fogarty catheter was compared with controls (CO) using intravital epifluorescence-microscopy over 4 h after BD induction; functional capillary density (FCD), leukocyte adherence (AL) in post-capillary venules, histology and pancreatic enzymes were investigated. Four hours after BD, FCD decreased (333 ± 11 vs. baseline 444 cm/cm 2 ± 5 SEM; p < 0.01) and showed lower values than CO (388 ± 9 p < 0.01). In BD, AL was increased (628 cells/mm 2 ± 110 SEM vs. baseline 123 ± 32, and vs. CO 180 ± 33; p < 0.001). BD caused increased histological damage (CO 1.6 scorepoints ± 0.7 SD vs. BD 8.3 ± 7.1; p < 0.05). Amylase was higher in BD (p < 0.05) but did not reach pathological values. We show for the first time that BD causes relevant changes in pancreatic microcirculation, histology and leukocyte endothelial interaction which might have a serious impact on the function of grafts. New strategies for preventing this damage are therefore highly desirable in order to improve the outcome of pancreas transplantation.

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Section: Discussionmentioning

confidence: 99%

Brain Death Impairs Pancreatic Microcirculation

Obermaier

Dobschuetz

Keck

et al. 2004

American Journal of Transplantation

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“…First, ischemic nontreated kidneys varied greatly in almost all parameters studied, including inflammation. Second, since the inflammatory response to I/R injury peaks 3-10 days after injury, 41,42 there is no guarantee that the 7th day after I/R is the optimal moment when inflammation is fully expressed.…”

Section: Discussionmentioning

confidence: 99%

Direct electrotransfer of hHGF gene into kidney ameliorates ischemic acute renal failure

et al. 2005

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“…In addition, T cell associated cytokines, such as IFN-y and TNF-a are produced [93] and blockade of the C28-B7 costimulatory pathway decreased early influx of T cells and expression of T cell associated cytokines [207]. We showed that cyclosporine was able to overcome the deleterious effects of ischemia in syngeneic transplants with a concomitant decrease in infiltrating CD4' T-cells [104].…”

Section: Endothelial Cell Activationmentioning

confidence: 99%

Etiology and pathophysiology of chronic transplant dysfunction

Kouwenhoven

IJzermans

Bruin

2000

Transplant International

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Chronic transplant dysfunction (CTD) is the predominant cause of late graft failure. The common histopathological feature in all transplanted organs is intimal hyperplasia accompanied by organ specific lesions. The knowledge about CTD is incomplete, and there is no therapy to prevent or treat it. This review describes the current knowledge on the etiology of CTD, with emphasis on kidney transplants, and postulates a pathophysiologic route through which CTD may develop. The problem of chronic transplant dysfunctionSince it was first shown in 1954 that successful transplantation of a healthy kidney could completely rehabilitate an individual with renal failure, transplantation of several organs has become an increasingly successful medical treatment for patients with end-stage organ failure. In 1998, in the Eurotransplant area alone, more than 3000 kidneys, 750 hearts, about 1000 livers, 230 lungs, and about 100 pancreas from cadaveric donors were transplanted [9]. Worldwide, 56 intestinal transplantations were performed in 1996 [70]. The shortterm results after clinical organ transplantation have improved progressively. This is principally due to refinements in tissue typing, advancements in organ preservation, operative techniques and ancillary care, more effective immunosuppressive agents, and better monitoring after engraftment. For example, one year survival of cadaveric kidneys has increased from approximately 50 % by the end of the 1960 s, to about 85 % nowadays 1671, and for living-related kidneys from 80% to Despite improving early results, however, it has become clear that clinical transplantation has not achieved its goal as a long-term treatment. For the period beyond one year, the annual rate of graft loss has changed less since the beginning of the experience. The half-life of cadaveric kidney allografts, for instance, has remained consistent at 7.5-9.5 years, although the latest United States Renal Data System (USRDS) data suggest that half-life of first cadaveric kidney grafts is improving (Figure 1) [68, 1461. Similarly, the half-life beyond the first year of heart transplants is 10.5 years [146]. Other organ transplants generally show comparable results, with exception of the liver, which shows more favourable long-term results [lo, 981.

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The role of the B7 costimulatory pathway in experimental cold ischemia/reperfusion injury.

Cited by 212 publications

References 34 publications

Brain Death Impairs Pancreatic Microcirculation

Brain Death Impairs Pancreatic Microcirculation

Direct electrotransfer of hHGF gene into kidney ameliorates ischemic acute renal failure

Etiology and pathophysiology of chronic transplant dysfunction

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