Acute liver allograft rejection and liver function: quantitative evaluation using the [14C]aminopyrine breath test.
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Acute Disease↗
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Exogenous IL-10 overexpression reduces perforin production by activated allogenic CD8+ cells and prolongs cardiac allograft survival.
Perforin is a cytolytic mediator produced by cytotoxic T cells (CD8(+) cells) and natural killer cells. We previously reported that ex vivo IL-10 gene therapy induced apoptosis of allogenic infiltrative CD8(+) cells and significantly prolonged cardiac allograft survival. To further test the hypothesis that localized IL-10 overexpression in cardiac allografts may also effect the alloreactive CD8(+) T cell function by downregulating its perforin production, we used a rabbit functional heterotopic allograft heart transplant model. Human recombinant IL-10 gene complexed with liposome was intracoronary delivered into the cardiac allografts ex vivo. The percentage of apoptotic infiltrative CD8(+) cells in cardiac allografts was increased 6-fold in the gene therapy group vs. the control group, whereas the percentage of perforin-positive CD8(+) cells was decreased 2.9-fold (P < 0.01). Perforin expression level in the allograft myocardium of the gene therapy group was deceased 3.2-fold (P < 0.01). The amount of infiltrative perforin-positive CD8(+) cells and perforin expression level were inversely correlated with IL-10 transgene and protein expression level in the myocardium of cardiac allografts (P < 0.01), the percentage of apoptotic cardiac myocytes (P < 0.01), and the peak left ventricular systolic pressure of cardiac allografts (P < 0.01) but significantly correlated with the infiltrative T cell cytotoxicity (P < 0.01) and allograft rejection score (P < 0.01). These results suggest that localized IL-10 gene therapy prolongs cardiac allograft survival, at least in part, through downregulation of perforin production by activated allogenic CD8(+) T cells. Reduction of cytolytic function of cytotoxic effector cells prevents the apoptosis of cardiac myocytes.
Animals↗
Comparison of tacrolimus and cyclosporin in renal transplantation by the protocol biopsies.
Acute and chronic lesion scores on renal allograft protocol biopsies may predict long-term graft function. The aim of this study was to compare the effects of tacrolimus (Tac) and cyclosporine microemulsion (CsA) based immunosuppressive protocols using protocol biopsies from well-functioning renal allografts. 35 consecutive renal transplant patients were randomized to Tac (n: 17) versus CsA (n: 18) treatment arms. Patient age and sex, donor type and age, histocompatibility, cold ischemia time and prior delayed graft function were similar between the two groups. Treatment protocol consisted of prednisolone, azathioprine and Tac or CsA. Biopsies performed on the third, sixth and twelfth months were blindly evaluated by the same pathologist. The incidences of acute rejection (AR) episodes among CsA vs Tac groups were 33% vs 29%, respectively (NS). The Creatinine level was lower in Tac than CsA, although it was not significant (Table). Subclinical AR and subclinical chronic allograft nephropathy were detected on protocol biopsies in 3 (2 CsA, 1 Tac) and 12 (7 CsA, 5 Tac) patients, respectively. Acute lesion score at the third month PBx was significantly lower in the Tac group (p < 0.05). Chronic lesion scores in all biopsies were lower in the Tac group, although not significantly. The protocol biopsy findings suggest that graft injury may be less pronounced among the Tac group.
Adult↗
Identification and treatment of cyclosporine-associated allograft thrombosis.
Endothelial injury associated with cyclosporine (CSA) therapy in the absence of rejection has resulted in irreversible intrarenal allograft thrombosis and transplant loss. Indium 111 (111In)-labeled platelet scanning is an effective way to identify those transplants that are at risk for acute loss. Two hundred prospective 111In scans were obtained (100 on allografts with normal function and 100 with transplant dysfunction of all causes). 111In scans in patients with dose-dependent CSA nephrotoxicity (N = 58) and biopsy proved acute rejection (N = 22) were negative. Grossly abnormal scans (three to eight times greater than hepatic uptake) were noted in nine recipients identified as having a hemolytic uremic-like syndrome associated with CSA use. Accelerated allograft functional loss was irreversible in six patients despite stopping CSA, systemic anticoagulation, increased steroids and antilymphocyte globulin, and infusion of fresh-frozen plasma. Three patients with grossly positive 111In scans and clinical and laboratory parameters consistent with this syndrome were treated with cessation of CSA and intra-arterial infusion of streptokinase into the renal allograft followed by systemic heparinization. Normal transplant function was regained and continues at 1, 7, and 8 months after transplant. 111In-labeled platelet scanning can noninvasively identify this syndrome of CSA-associated arteriopathy and allow for early therapy to reverse it. Intrarenal arterial streptokinase therapy is a successful way to treat acute CSA-associated arteriopathy.
Blood Platelets↗
[TGF-beta1 in allograft and long-term renal function].
OBJECTIVE: To determine the relation between transforming growth factor beta1 (TGF-beta1) in allograft and long-term renal function. METHODS: Urine TGF-beta1 relative concentration (divided by urine creatinine) was tested in 168 recipients whose renal function was normal between August 1, 2000 and March 31, 2001. Twenty patients with higher urine TGF-beta1 relative concentrations formed Group A, and another 20 patients with lower urine TGF-beta1 formed Group B. In both groups biopsies were carried out in 15 cases and 12 cases respectively, and TGF-beta1 in the biopsis was tested by immunofluorescence. Blood TGF-beta1 concentrations in the 2 groups were also tested. Three years later, the renal function was compared between the 2 groups. Biopsies were carried out in renal recipients whose creatinine was higher than that of the normal. RESULTS: Blood TGF-beta1 concentrations in the 2 groups were not different significantly; 3 years after the transplantation, there was more loss of renal function and more chronic allograft nephropathy (CAN) cases in Group A than in Group B. Expression of TGF-beta1 in the allografts was higher in Group A than in Group B. The differences in the 2 groups were significant. CONCLUSION: The findings suggest that the higher expression of TGF-beta1 in the allografts is associated with the lower long-term survival rate of kidney graft. The level of urine TGF-beta1 after the renal transplantation can predict the long-term renal function.
Biopsy, Needle↗
Donor-specific IgG antibody and the chronic rejection of human renal allografts.
Although many investigators have felt that humoral antibody was responsible for chronic rejection, attempts to detect it in the sera of recipients in the presence of functioning renal allografts have been largely unsuccessful. A modification of the mixed antiglobulin reaction has increased its sensitivity so that the development of low titers of immunoglobulin (IgG) antibody antibody specific for donor kidney cells can be detected in renal allograft recipients while renal function is still good. Donor-specific antibody was detected in the sera of 11 of 13 patients whose transplants had ceased to function from 5 to 43 months after transplantation. In five recipients the antibody was present prior to as well as after transplantation and in six recipients antibody developed after transplantation from 3 to 25 months prior to the cessation of function. In the patients with antibody, chronic rejection was characterized by hypertension which required treatment with multiple drugs, by proteinuria of greater than one gram per day, by a gradual, progressively rising serum creatinine, and by an absence of acute ologuric rejection episodes. Pathologically there was extensive intimal proliferation and occlusion of the intrarenal arteris. There also was significant glomerulonephritis which consisted of thickening of the basement membranes, mesangial cell proliferation, simplification of the capillary loops, and in some patients fibroepithelial crescent formation. These findings suggest that IgG antibodies directed against cell-surface antigens of the donor are the chief cause of chronic renal allograft rejection.
Adult↗
Renal allograft histology and correlation with function in children on triple therapy.
Histopathological findings of 13 LRD and 17 CAD renal allografts of paediatric recipients were prospectively semiquantitatively scored and correlated with clinical and functional parameters 18 and 36 months after transplantation. The most common findings at 18 months were diffuse interstitial fibrosis (incidence 57%), glomerular mesangial matrix increase (91%), arteriolar intimal proliferation (70%), and tubular atrophy (83%). Most changes were mild and most biopsies were scored normal or borderline (Banff classification). At 18 and at 36 months 30% of grafts showed mild chronic rejection (CR). Only two grafts showed grade II CR at 18 months and one graft grade III CR at 36 months. Progressive CR was not seen. Donor source or recipient age had no effect on graft histology. Vascular-interstitial cyclosporin (CsA) nephrotoxicity was not found. On the contrary, cumulative CsA dose (mg/kg/day) showed an inverse correlation with arteriolar intimal proliferation (P < 0.001). 51Cr-EDTA and lithium clearances showed inverse correlations with diffuse interstitial fibrosis and lymphocytosis. PAH clearance did not correlate with interstitial or vascular changes. The results indicate good prognosis in children on triple immunosuppression (with CsA administered in three doses/day to pre school children) regardless of donor source.
Adolescent↗
Cryopreserved aortic allografts for aortic root reconstruction: a single institution's experience.
BACKGROUND: An evaluation of early and long-term results of aortic root replacement with cryopreserved aortic allografts and echocardiographic follow-up of allograft valve function was performed. METHODS: From September 1989 through May 1998, 132 patients aged 17 to 77 years (mean, 50.8 +/- 14.8 years) underwent freestanding aortic root replacement with a cryopreserved aortic allograft. Eighty-six (65.1%) patients had New York Heart Association class III or IV functional status before operation, and 27 (20.5%) patients underwent emergency operation. Fifty-nine (44.7%) patients had undergone previous cardiac operations. The cause of aortic disease was acute endocarditis in 63 (47.7%) patients, healed endocarditis in 15 (11.3%), degenerative in 20 (15.2%), congenital in 20 (15.2%), failed prosthesis in 10 (7.6%) and rheumatic in 4 (3.0%). Follow-up was complete, with a mean of 42 months. RESULTS: There were 12 hospital deaths (9.1%; 70% confidence limits [CL], 6.6% and 11.6%); 9 of them were operated on for active endocarditis (p = 0.062). Multivariate analysis determined age older than 65 years (p = 0.012) and emergency operation (p = 0.009) as independent risk factors for hospital mortality. During follow-up, 6 (5.0%; 70% CL, 3.0% and 7.0%) patients died. Cumulative survival rate for the entire group was 81.8% +/- 5.4% at 8 years. Freedom from reoperation for structural valve failure was 100%, freedom from reoperation for any cause was 96.3% +/- 1.8% at 8 years. Freedom from endocarditis at 8 years was 97.9% +/- 1.4%. Follow-up of allograft valve function showed no or trivial aortic regurgitation in 97% of patients and absence of stenosis of the allograft in 100%. CONCLUSIONS: Aortic root replacement with cryopreserved aortic allografts can be performed with acceptable hospital mortality and long-term results. The durability of cryopreserved aortic allografts is good, and reoperation for structural valve failure is absent at 8 years.
Adolescent↗
In vitro evidence for defective afferent immune function in long-term renal allograft recipients.
Experiments were designed to evaluate afferent immune functions in 21 long-term (greater than or equal to 3 years) renal allograft recipients by using in vitro assays that included autologous and allogeneic mixed lymphocyte reactions (AMLR and allo-MLR), proliferative responses to a soluble antigen (tetanus toxoid), and the ability to generate cytotoxic T lymphocytes (CTL) following stimulation in an AMLR. The results showed that allograft recipients generated responses in the allo-MLR (means = 84,789 +/- 8242) that were comparable to those exhibited by normal controls (means = 86,082 +/- 7423). Likewise, mean responses in the AMLR were similar in recipients and controls (14,937 +/- 3243 versus 16,101 +/- 3005), although a greater percentage of recipients generated AMLRs below 5000 cpm than did normals (8/21 versus 4/20). However, 13 recipients analyzed for responsiveness to tetanus toxoid were shown to generate mean proliferative responses that were significantly depressed below normal (18,095 +/- 5545 versus 48,935 +/- 8813, P less than 0.001). Furthermore, despite significant proliferation in the AMLR means = 27,648 +/- 5168), 8 recipients generated significantly lower CTL activity in AMLR cultures than normal controls (mean percentage of cytotoxicity = 10.3 +/- 4.7 versus 24.9 +/- 4.7, P less than 0.05). These recipients generated normal CTL levels against allogeneic target cells following stimulation in an allo-MLR. Thus, these studies provide experimental support for the existence of altered T helper cell-mediated functions in long-term renal allograft recipients.
Humans↗
Aortic valve graft implantation in rats: a new functional model.
BACKGROUND: Allograft heart valves used in cardiac surgery often fail at an unacceptable rate. Immune mechanisms contribute to this failure, but adequate and functional small-animal valve models to characterize this phenomenon are lacking. The objective of this study was to create native aortic valve insufficiency in recipient rats to provide for a functional abdominal aortic valve graft implant. METHODS: Lewis recipient rats underwent single-leaflet injury of their native aortic valve through a right carotid catheter injury. Animals were allowed to recover for 28 days, at which time a Lewis aortic valve graft was implanted infrarenally. Echocardiography with color flow Doppler scanning was performed before aortic injury, 1 week after aortic injury, and after abdominal implantation of a valve graft in animals with native aortic insufficiency. RESULTS: After aortic valve injury, all animals had moderate-to-severe aortic insufficiency with a significant increase in diastolic and systolic left ventricular dimensions. Color flow Doppler scanning revealed diastolic aortic flow reversal from the aortic valve extending to the infrarenal abdominal aorta. Aortic valve grafts were then implanted infrarenally in animals with created aortic valve insufficiency and resulted in 100% patency and preservation of leaflets at 4 weeks after implantation. Leaflet motion of the abdominal graft was visualized by means of M-mode echocardiography. CONCLUSION: Compensated native aortic insufficiency results in aortic diastolic flow reversal distal to the infrarenal aorta, thus allowing normal motion of the infrarenal allograft leaflets. This functional model will provide an opportunity to investigate the role of immunologic valve injury in the failure of valve allografts.
Animals↗
Pattern of graft- and host-specific MHC class II expression in long-term murine cardiac allografts: origin of inflammatory and vascular wall cells.
In solid-tissue allografts, donor vascular cells as well as recipient inflammatory cells can express MHC class II molecules. However, it is uncertain how much residual donor endothelium persists and to what extent donor versus recipient MHC class II expression can contribute to the ongoing immune response, especially in long-term grafts. To establish the origin of class-II-expressing cells in the allograft, we evaluated the expression of donor- or recipient-specific MHC class II molecules in murine cardiac allografts. Donor hearts from BALB/c (H-2d) mice were transplanted into C57BL/6 (B6, H-2b) recipients; B6 isografts served as controls. Untreated allografts ceased functioning at approximately 7 days with severe parenchymal rejection. Allografts from recipients treated with anti-CD4 and anti-CD8 MAbs after transplantation were explanted at 8 to 12 weeks and demonstrated intimal fibroproliferative lesions with a mild parenchymal mononuclear cell infiltrate. Class II expression in isografts was limited to epicardial macrophages. Both acutely rejecting and long-term allografts contained abundant macrophages expressing recipient class II molecules. Occasional cells (passenger leukocytes) in untreated, acutely rejecting allografts bore donor class II molecules; long-term allografts contained few such cells. In contrast, vascular endothelial and medial smooth muscle cells consistently expressed donor class II molecules. These results suggest that ongoing MHC class II expression in donor vascular cells, as well as in recipient macrophages, may contribute to sustained activation of host T cells with consequent release of cytokines that ultimately promote the development of graft arteriosclerosis.
Actins↗
Decrease in natural killer cell activity in kidney allograft recipients.
The natural killer cell activity (NKCA) of a population of 66 functioning kidney allograft recipients (followed up for over 9 years) was assessed on K562 and DORA cell line targets. The 51Cr specific release test showed a rapid, sharp decrease in NKCA as early as 3 months after grafting, reaching a minimal level between 7 and 60 months (5 +/- 5 vs. 45 +/- 19% 51Cr release; P less than 0.001). Patients showing an almost total lack of NKCA were roughly the same whether assessed on K562 or DORA targets. NKCA tended to be restored in long-term transplanted patients (greater than 61 months). Control populations, aside from 32 healthy individuals, consisted of 11 haemodialysed patients as well as patients submitted to corticosteroid therapy for more than one year (8 cases of giant cell arteritis and 4 chronic asthmas). Haemodialysed patients exhibited normal NKCA (whether previously grafted or not). Corticosteroid-treated patients showed either no significant modification (K562 target) or a borderline decrease (DORA target) in NKCA. Azathioprine or corticosteroid dosage intake on the day of the test did not influence the level of graft recipient NKCA. The natural cytotoxicity of peripheral blood lymphocytes (PBL) from recipients lacking in activity (less than 5% 51Cr release) was not restored by exogenous (type alpha) interferon. and PBL of recipients with low NKCA scores produced normal levels of purified interferon after 24-h Sendai virus exposure. No inhibitory effects of sera obtained from recipients lacking NKCA nor any active suppressor cells from their PBL could be evidenced, thus suggesting an actual loss of natural killer progenitors (or an "insensitivity" to interferon) in those patients. Corticosteroids, as opposed to azathioprine, were able to decrease the in vitro NKCA of healthy donor PBL at pharmacological concentrations.
Adult↗
Increased expression of transforming growth factor-beta and eosinophil infiltration is associated with the development of transplant arteriosclerosis in long-term surviving cardiac allografts.
BACKGROUND: Transplant arteriosclerosis is a major limiting factor for long-term function of allografts in clinical transplantation. This study investigated the impact of three different protocols capable of inducing long-term allograft survival on the development of transplant arteriosclerosis and immune response in cardiac allografts. METHODS: CBA.Ca (H2k) recipients of fully allogeneic C57/BL10 (H2b) heart grafts received a short-term course of anti-CD154 antibody or were pretreated with anti-CD4 antibody in combination with donor alloantigen in the form of CBK (H2k+Kb) bone marrow or C57BL/10 donor-specific transfusion (DST). Grafts were analyzed on day 40 or 100 after transplantation for transplant arteriosclerosis and expression of interferon-gamma, interleukin (IL)-2, IL-4, IL-10, IL-12p40, inducible nitric oxide synthase, and transforming growth factor (TGF)-beta1 mRNA. Serum was analyzed for the presence of alloantibodies. RESULTS: Intimal proliferation was 62%+/-11% on day 40 in the anti-CD154 group, progressed from 31%+/-10% on day 40 to 68%+/-8% on day 100 in the CBK-bone marrow group, but remained stable at 39%+/-4% in the DST group. Increased transplant arteriosclerosis on day 100 was associated with high intragraft TGF-beta1 mRNA production and eosinophil infiltration, but not alloantibody production. Progressing transplant arteriosclerosis was associated with increased IL-4 expression. CONCLUSION: Treatment protocols for the induction of long-term allograft survival can differ substantially in the extent and kinetics of transplant arteriosclerosis. IL-4 and TGF-beta1 may be two potential therapeutic targets to attenuate the development of transplant arteriosclerosis in the long term.
Animals↗
[Phenotypic and functional analyses of cells infiltrating rat hepatic allograft].
In order to elucidate the immunological characteristics of rat liver transplantation, graft infiltrating cells (GIC) were isolated from rat hepatic allografts, and phenotypic and functional analyses were performed. Long-surviving combination (Lewis engrafted BN liver, MST = 166.8 +/- 28.1 days, n = 10) and acutely-rejected combination (Lewis engrafted DA liver, MST = 9.6 +/- 0.3 days, n = 6) were compared. Relative proportions of all T cells and activated T cells assessed by flow cytometry were significantly higher in Lewis recipients of acutely-rejected combination than in those of long-surviving combination on day 6 after transplantation. Phenotypic analyses of GIC on days 6, 14, and 45 after transplantation in Lewis hosts of long-surviving combination were assessed. All T cells, OX-8 positive cells (Tc/s, NK), and OX-39 positive (IL-2 receptor) cells showed peak levels on day 6 and decreased on day 45. Cytotoxic activity of GIC toward donor lymphocytes on day 6 was stronger in host of acutely-rejected combination (18.9 +/- 4.0%, E/T = 50) than in that of long-surviving combination (5.3 +/- 2.8%). On the other hand, NK activity in Lewis host of long-surviving combination was high (17.5 +/- 3.0%, E/T = 100) on day 6 after transplantation. These results demonstrate that some immunosuppressive mechanism is present already on day 6 after transplantation, and that infiltration or activation of cytotoxic T cells is inhibited in long-surviving combination of rat hepatic allografts.
Animals↗
Insulin-like growth factor-I (IGF-I) and glutamine improve structure and function in the small bowel allograft.
IGF-I, a mitogenic polypeptide hormone, and glutamine (GLN), the preferred enterocyte fuel, singularly improve growth and structure of the small bowel isograft; however, their combined effects on intestinal allografts are unknown. This study examined the effects of IGF-I and GLN, singularly and in combination, on the structure and function of the intestinal allograft. Fifty-nine adult rats underwent resection of the distal 60% of small bowel and received either a 40-cm isograft or an allograft. Either IGF-I (2.4 mg/kg/day) or its vehicle was infused continuously by subcutaneous minipumps. An isocaloric polymeric diet with either 2% GLN or isonitrogenously balanced 2% nonessential amino acids was given continuously by gastrostomy for 10 days. Five groups were studied: isograft (ISO) alone, allograft (ALLO) alone, ALLO and GLN, ALLO and IGF-I, and ALLO and IGF-I with GLN. All recipients received Cyclosporine A (15 mg/kg, im) daily. Mucosal villus height, surface area, crypt depth, IgA, IgG, IgM, and intercellular adhesion molecule-1 (ICAM-1) plasma cells in intestinal tissue, glucose and water absorption of intestinal graft, bacterial translocation (BT) to mesenteric lymph nodes, and body weight were determined. IGF-I increased villus height, surface area (P < 0.001), crypt depth (P < 0.01), and glucose absorption (P < 0.05) compared to the ISO and ALLO groups. GLN increased only crypt depth when compared to the ALLO group (P < 0.01). Both IGF-I and GLN independently decreased BT to MLN (P < 0.05) and, in combination, enhanced water absorption (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Vitamin C improves endothelial dysfunction in renal allograft recipients.
BACKGROUND: Endothelial function is impaired in renal allograft recipients but the effects of antioxidant vitamin therapy on endothelial function in such patients is unknown. METHODS: Thirteen renal allograft recipients were randomized to vitamin C or placebo in a double blind cross-over study design. Flow-mediated endothelium-dependent dilation and glyceryltrinitrate-induced endothelium-independent dilation of the brachial artery were assessed before and 2 h after oral administration of 2 g vitamin C or placebo. RESULTS: Plasma vitamin C levels increased from 33.5+/-17.0 micromol/l to 98.8+/-60.2 micromol/l after treatment (P=0.0001). Endothelium-dependent dilation improved (from 1.6+/-2.6 to 4.5+/-2.5%) after vitamin C administration but was unchanged after placebo (1.9+/-1.5 to 1.8+/-2.5%; P=0.003 for vitamin C vs placebo). There was no significant change in endothelium-independent dilation in response to vitamin C. Vitamin C was also associated with a significant increase in the lag time in dilute serum oxidation (P=0.001). CONCLUSIONS: Vitamin C acutely improves flow-mediated, endothelium-dependent dilation and increases the resistance of lipoproteins in dilute serum to oxidation in renal transplant recipients.
Ascorbic Acid↗
Role of tumor necrosis factor receptors TNFR-I (P55) and TNFR-II (P75) in corneal transplantation.
BACKGROUND: To determine the role of tumor necrosis factor-alpha (TNF-alpha) receptor (TNFR) function in corneal allograft immunology. METHODS: Animals with gene-targeted deficiency in TNFR-I (p55-/-), TNFR-II (p75-/-), or combined TNFR-I/TNFR-II deficiency (p55-/-p75-/-) and their wild-type controls were used as recipients of fully-mismatched (BALB/c; n=88) or multiple minor alloantigen-mismatched (BALB.b; n=62) orthotopic corneal transplants to determine the effect of selective deficiency in one or both TNF-alpha receptors on corneal allograft survival. Grafted recipients were followed biomicroscopically for signs of rejection, and survival data were analyzed by the Kaplan-Meier method. RESULTS: There was no discernible difference in survival of fully-mismatched BALB/c corneal grafts in p55-/- (n=12; P=0.76) or in double-knockout p55-/-p75-/- (n=13; P=0.41) as compared with wild-type C57BL/6.129 hosts. However, the survival of BALB/c allografts was lower in p75-/- (n=10; median survival 20 days) as compared with control C57BL/6 (n=30; median survival 30 days) hosts (P=0.02). In contrast, there was no discernible effect in survival of minor alloantigen-disparate BALB.b corneal grafts in p75-/- (n=13; P=0.95) or in combined p55-/-p75-/-(n=10; P=0.17) hosts as compared with C57BL/6 (n=9) and C57BL/6.129 (n=10) wild-type controls, respectively. However, there was a profound enhancement in the survival of BALB.b allografts in p55-/- recipients (n= 10; median survival 35 days) as compared to wild-type C57BL/6.129 (n=10; median survival 25 days) controls (P<0.01). CONCLUSIONS: Our data suggest that the two TNF-alpha receptors largely play discrete roles in mediating rejection of murine corneal allografts. TNFR-I (p55) function seems to be integral to the rejection of minor-disparate grafts, and its selective suppression leads to enhancement of allograft survival. In contrast, TNFR-II (p75) function appears to be associated with enhanced survival of major histocompatibility complex-disparate allografts. The combined deletion of TNFR functionality in p55-/-p75-/- confers no net advantage or disadvantage to major histocompatibility complex or minor alloantigen-disparate grafts.
Animals↗
Improved pregnancy outcome in a patient with renal allograft nephropathy undergoing temporary hemodialysis.
We report a case of a woman with a poorly functioning renal allograft and a positive anti-cardiolipin antibody who was dialysis-independent and conceived 18 months following her transplant. She was electively maintained on hemodialysis during the pregnancy and delivered a live infant at 31 weeks gestation. Her renal function returned to prepregnancy levels post partum and she remained dialysis-independent.
Adult↗