Log in

Relevant bibliographies by topics / Graft rejection

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Academic literature on the topic 'Graft rejection'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Graft rejection.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Graft rejection"

1

van Agteren, Madelon, Willem Weimar, Annelies E. de Weerd, Peter A. W. te Boekhorst, Jan N. M. Ijzermans, Jaqueline van de Wetering, and Michiel G. H. Betjes. "The First Fifty ABO Blood Group Incompatible Kidney Transplantations: The Rotterdam Experience." Journal of Transplantation 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/913902.

Full text

Abstract:

This study describes the single center experience and long-term results of ABOi kidney transplantation using a pretransplantation protocol involving immunoadsorption combined with rituximab, intravenous immunoglobulins, and triple immune suppression. Fifty patients received an ABOi kidney transplant in the period from 2006 to 2012 with a follow-up of at least one year. Eleven antibody mediated rejections were noted of which 5 were mixed antibody and cellular mediated rejections. Nine cellular mediated rejections were recorded. Two grafts were lost due to rejection in the first year. One-year graft survival of the ABOi grafts was comparable to 100 matched ABO compatible renal grafts, 96% versus 99%. At 5-year follow-up, the graft survival was 90% in the ABOi versus 97% in the control group. Posttransplantation immunoadsorption was not an essential part of the protocol and no association was found between antibody titers and subsequent graft rejection. Steroids could be withdrawn safely 3 months after transplantation. Adverse events specifically related to the ABOi protocol were not observed. The currently used ABOi protocol shows good short and midterm results despite a high rate of antibody mediated rejections in the first years after the start of the program.

APA, Harvard, Vancouver, ISO, and other styles

2

Petra, Hřibová, Honsová Eva, Brabcová Irena, Hrubá Petra, and Viklický Ondřej. "Molecular Profiling of Acute and Chronic Rejections of Renal Allografts." Clinical and Developmental Immunology 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/509259.

Full text

Abstract:

Both antibody mediated (AMR) and T-cell mediated (TCMR) rejections either acute or chronic represent the main reason for late graft dysfunction. In this study we aimed to evaluate differences in the intrarenal expression patterns of immune system related genes in acute and chronic rejections. Graft biopsies were performed and evaluated according to Banff classification. Using the TaqMan Low Density Array, the intrarenal expressions of 376 genes relating to immune response (B-cell activation, T-cell activation, chemokines, growth factors, immune regulators, and apoptosis) were analyzed in the four rejection categories: chronic AMR, chronic TCMR, acute AMR, and acute TCMR. The set of genes significantly upregulated in acute TCMR as compared to acute AMR was identified, while no difference in gene expressions between chronic rejections groups was found. In comparison with functioning grafts, grafts that failed within the next 24 months after the chronic rejection morphological confirmation presented at biopsy already established severe graft injury (low eGFR, higher proteinuria), longer followup, higher expression of CDC20, CXCL6, DIABLO, GABRP, KIAA0101, ME2, MMP7, NFATC4, and TGFB3 mRNA, and lower expression of CCL19 and TRADD mRNA. In conclusion, both Banff 2007 chronic rejection categories did not differ in intrarenal expression of 376 selected genes associated with immune response.

APA, Harvard, Vancouver, ISO, and other styles

3

Suhorukovs, Vadims, and Tatjana Tihomirova. "Impact of Subclinical Acute Rejection on Renal Graft Function: Results of Three-Year Follow-Up." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences 67, no. 1 (April 1, 2013): 42–46. http://dx.doi.org/10.2478/prolas-2013-0008.

Full text

Abstract:

Notwithstanding that in the last years the immediate results of kidney transplantation have been improved, there has been no adequate improvement of long-term results. Therefore, more attention is being paid to the so-called subclinical rejections of renal grafts, detected by protocol biopsies, as a possible factor affecting renal function in late period. The aim of this study was to determine the frequency of subclinical rejections and their impact on further renal graft function. Within the frame of the study 40 protocol biopsies were performed in 26 patients with immediate and stable renal graft function. In 17 (65.4%) of them a subclinical rejection of IA-IIA degree was detected. In nine patients with subclinical rejection, treatment with steroids was applied, while eight recipients did not receive any additional therapy. In follow-up, in a period of three years there was no statistically significant difference in blood creatinine level, glomerular filtration rate, number of clinical rejections during the monitoring period, and three-year survival of the transplanted kidney in patients, regardless of where the treatment of subclinical rejection was applied. The results of our study did not indicate any impact of subclinical rejection on renal graft function in the late post-operation period.

APA, Harvard, Vancouver, ISO, and other styles

4

Bolton, E. M., J. A. Gracie, J. D. Briggs, J. Kampinga, and J. A. Bradley. "Cellular requirements for renal allograft rejection in the athymic nude rat." Journal of Experimental Medicine 169, no. 6 (June 1, 1989): 1931–46. http://dx.doi.org/10.1084/jem.169.6.1931.

Full text

Abstract:

This study has examined the ability of adoptively transferred CD4+ and CD8+ T cells to mediate rejection of a fully allogeneic DA renal graft in the PVG nude rat. Transfer, at the time of transplantation, of naive CD4+ T cells caused rapid graft rejection and primed CD4+ cells were several times more potent. In contrast, naive or specifically sensitized CD8+ cells were entirely ineffective at mediating renal allograft rejection. Whereas nonrejecting grafts showed only a mild cellular infiltrate, rejecting grafts in CD4+ reconstituted animals showed a substantial infiltrate and many of the infiltrating cells had a phenotype (MRC OX8+, MRC OX19-), consistent with NK cells. Experiments using a mAb (HIS 41) against an allotypic determinant of the leukocyte common antigen confirmed that the majority (greater than 80%) of the cellular infiltrate in rejecting grafts derived from the host rather than from the CD4+ inoculum. Infiltrating mononuclear cells, obtained from rejecting allografts 7 d after transplantation in CD4+-injected PVG nude hosts, showed high levels of in vitro cytotoxicity against not only kidney donor strain Con A blasts but also third-party allogeneic Con A blasts, as well as against both NK and LAK susceptible targets. When splenocytes from nontransplanted nude PVG rats were tested in vitro they also demonstrated high levels of lytic activity against both NK and LAK susceptible targets as well as allogeneic Con A blasts, which were not susceptible to lysis by spleen cells from euthymic rats. These findings suggest that injected CD4+ cells may cause renal allograft rejection by the recruitment of extrathymically derived, widely alloreactive cells into the kidney in this model of graft rejection.

APA, Harvard, Vancouver, ISO, and other styles

5

Dennert, G., C. G. Anderson, and J. Warner. "T killer cells play a role in allogeneic bone marrow graft rejection but not in hybrid resistance." Journal of Immunology 135, no. 6 (December 1, 1985): 3729–34. http://dx.doi.org/10.4049/jimmunol.135.6.3729.

Full text

Abstract:

Abstract Results of recent experiments have provided compelling evidence supporting the hypothesis that the acute rejection of bone marrow transplants by allogeneic and semiallogeneic recipients is principally due to the action of natural killer (NK) cells. The observed specificity of graft rejection is likely induced by target-specific antibody that guides the NK cells in an antibody-dependent cytolytic reaction resulting in the elimination of the graft. The sole involvement of NK cells in marrow graft rejection, however, is contradicted by several observations that point to the environment of specific T cells. Results presented in this paper demonstrate that in allogeneic marrow graft rejection models, T killer cells are capable of causing graft rejection provided a prior sensitization phase is allowed. Thus, mice not able to reject marrow grafts in a primary response via their NK cells will do so in a primed secondary response via their T cells. Rejection is specific in that only marrow grafts H-2 identical to the sensitizing marrow graft are rejected. Sensitization for NK cell independent marrow graft rejection can be accomplished by prior priming with allogeneic tumor cells or by injection of cloned T killer cells. In contrast to bone marrow allograft rejection, the hybrid resistance model in which F1 hybrid mice reject parental marrow grafts does not appear to induce T killer cells in vivo. Neither marrow grafts nor tumor cells prime F1 hybrids for a second-set parental graft rejection. Moreover, F1 hybrid antiparental T killer cells induced in vitro and adoptively transferred in vivo fail to transfer hybrid resistance. Therefore, there appear to be potent mechanisms acting in vivo that suppress the action or induction of F1 hybrid T killer cells specific to parental antigens.

APA, Harvard, Vancouver, ISO, and other styles

6

Tullo, A. B. "Graft rejection." Eye 12, no. 4 (July 1998): 609–10. http://dx.doi.org/10.1038/eye.1998.152.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Allocco, Jennifer Brianne, Christine McIntosh, Peter Wang, Michelle McKeague, Ying Wang, Alexandra Cassano, Stephen Z. Xie, et al. "Variegated levels of alloreactive T cell dysfunction in transplantation tolerance determine graft vulnerability to infection-triggered rejection." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 173.08. http://dx.doi.org/10.4049/jimmunol.210.supp.173.08.

Full text

Abstract:

Abstract While advances have been made in therapies that achieve tolerance in mouse models of transplantation, successful tolerance remains vulnerable to inflammatory insults, which can trigger graft rejection. To identify strategies for improving the robustness of tolerance, we aim to better understand the mechanisms by which grafts are rejected after donor-specific tolerance is established. In a mouse model of cardiac allograft tolerance in which late infection with Listeria monocytogenes (Lm) can trigger graft rejection, we previously showed that host CD4 +T cells reactive to host MHC-II presenting a donor MHC-I-derived peptide (TCR75 cells) became intrinsically dysfunctional if the alloantigen persisted for 3 weeks or greater. Intriguingly, infection-dependent transplant rejection was not associated with transcriptional or functional reinvigoration of these cells. We hypothesized that there might be heterogeneity in the level of dysfunction of alloreactive T cells depending on duration of their cognate alloantigen persistence. Unlike TCR75 cells, CD4 +T cells specific for host MHC-II presenting a peptide derived from donor MHC Class II (TEa cells), a graft antigen that declines post-transplantation, retained functionality during tolerance induction. Consequently, TEa but not TCR75 cells expanded following Lm-infection, supporting a role for TEa-like cells in driving infection-triggered rejection. Prolonging T cell exposure to cognate alloantigens aggravated TEa dysfunction and rendered grafts resistant to Lm-dependent rejection. These findings demonstrate that inducing dysfunction in a broader array of allospecific T cells, by prolonging exposure to more alloantigens, lessens graft vulnerability to infections. Supported by the UChicago Growth Development and Disabilities Training Program (T32 HD007009). AHA predoctoral fellowships (20PRE35210946, 3PRE14550022 and 15PRE22180007). NIH T32-AI007090. UChicago Cardiovascular Pathophysiology and Biochemistry Training Grant (T32 HL07237). HHMI Med-into-Grad Program training grant (56006772). NIAID Grant P01AI-97113.

APA, Harvard, Vancouver, ISO, and other styles

8

Onyema, Oscar Okwudiri, Yizhan Guo, Qing Wang, Andrew E. Gelman, Daniel Kreisel, Elizabeth A. Jacobsen, and Alexander Sasha Krupnick. "Eosinophils alleviate lung allograft rejection through their modulation of CD8+ T Cells." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 55.14. http://dx.doi.org/10.4049/jimmunol.200.supp.55.14.

Full text

Abstract:

Abstract Introduction Based on the accumulation of eosinophils (eos) in rejected lung grafts, it was widely held that eos perpetuate lung graft rejection. However, we showed recently in a mechanistic study that eos mediate lung graft tolerance. As eos are also present in rejected lungs, we therefore explore the possibility of a different role of eos in lung graft rejection. Method Using orthotopic left lung transplantation of MHC-1 mismatched Balb/c (H2Kd) donors to C57BL/6J (H2Kb) recipients, with or without co-stimulatory blockade immunosuppression, we quantified the number of eos in lung grafts at day 7 post-transplant (D7). Th1, Th2 and Th17 cytokine profiles of D4 lung grafts were analyzed by quantitative PCR. D7 eos were also analyzed for their expression of Th1, Th2 and Th17 signature genes. The role of eos was examined in iPHIL mice that experience selective ablation of eos after Diphtheria toxin (DT) administration. Balb/c left lungs transplanted into DT or vehicle treated iPHIL mice without immunosuppression were analyzed histologically and flow cytometrically at D4. Results We observed similar numbers of eos, higher Th1 polarization, lower IL33, a Th2 cytokine and less Th17 polarization of the lung microenvironment, and higher expression of the Th1 signature genes among eos, in rejecting compared to accepting lung grafts. Eos deficiency was associated with more rapid lung graft rejection, evidenced in higher CD8+ T cell proliferation, lower CD4/CD8 ratio, and enhanced T cell differentiation to effector memory phenotype. Conclusion Our results indicate that eos directly ameliorate lung graft rejection even in the absence of immunosuppression. This calls for a revalidation of the importance of eos in lung allograft pathology.

APA, Harvard, Vancouver, ISO, and other styles

9

Hall, B. M. "Mechanisms maintaining enhancement of allografts. I. Demonstration of a specific suppressor cell." Journal of Experimental Medicine 161, no. 1 (January 1, 1985): 123–33. http://dx.doi.org/10.1084/jem.161.1.123.

Full text

Abstract:

DA rats treated with hyperimmune anti-PVG serum and grafted with (DA X PVG)F1 heart grafts in which graft survival was prolonged for greater than 75 d were used to examine the cellular mechanisms that maintain the state of specific unresponsiveness found in these animals. The capacity of lymphocytes from these animals to effect or inhibit graft rejection on adoptive transfer to irradiated heart-grafted hosts was tested. Spleen cell populations and the T cell subpopulation separated from spleen cells in vitro failed to restore rejection of PVG heart grafts in irradiated DA recipients but restored third party Lew graft rejection. Whole spleen cells had the capacity to suppress the ability of normal DA LNC to cause graft rejection, but T cells from spleen only delayed the restoration of rejection. LNC and recirculating T cells from rats with enhanced grafts adoptively restored PVG rejection, however. These studies show that the state of specific unresponsiveness that follows the induction of passive enhancement is dependent in part upon active suppression, which is induced or mediated by T lymphocytes. The recirculating pool of lymphocytes in these animals is not depleted of specific alloreactive cells with the capacity to initiate and effect rejection. Thus, these animals' unresponsiveness is not like that found in transplantation tolerance induced in neonatal rats, but is, in part, due to a suppressor response that can inhibit normal alloreactive cells' capacity to initiate and effect rejection.

APA, Harvard, Vancouver, ISO, and other styles

10

Priftakis, P., G. Bogdanovic, G. Tyden, and T. Dalianis. "Polyomaviruria in Renal Transplant Patients Is Not Correlated to the Cold Ischemia Period or to Rejection Episodes." Journal of Clinical Microbiology 38, no. 1 (January 2000): 406–7. http://dx.doi.org/10.1128/jcm.38.1.406-407.2000.

Full text

Abstract:

ABSTRACT Polyomaviruria was observed in one-third of all renal transplant patients, irrespective of whether their renal grafts came from a living or cadaver donor, and was not correlated to graft rejection episodes. This suggests that the renal graft ischemia period is not the major cause of polyomavirus reactivation and that reactivation of polyomavirus is not a dominant cause of graft rejection.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Graft rejection"

1

Dooldeniya, Mohanta Deevan. "The role of graft expressed Fasligand in graft rejection." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419907.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Waters, Cheryl Denise. "The cellular requirements for graft rejection." Thesis, The University of Sydney, 1985. https://hdl.handle.net/2123/26737.

Full text

Abstract:

The studies described in this thesis were designed to develop a model in which the capacity of various lymphoid cells subpopulations to cause graft rejection could be tested and correlated with their capacity to effect in vitro lysis of appropriate target cells.

APA, Harvard, Vancouver, ISO, and other styles

3

Wu, Guosheng. "Experimental studies on xenograft rejection /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4805-4/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Patrick, Guy M. "Studies of cytokines in alloimmune responses /." Title page, table of contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09php314.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Kumar, Rajesh. "Does graft-expressed TRAIL modify the rejection process?" Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544289.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Duguid, I. G. M. "Prevention of corneal graft rejection with monoclonal antibodies." Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387460.

Full text

Abstract:

This thesis aims to place corneal allograft rejection in the context of general transplantation immunology, examine the role of lymphocyte subsets in the rejection process and consider the potential application of monoclonal antibody therapy in clinical corneal graft rejection. The literature relating to the current clinical practice of corneal grafting, with particular reference to corneal allograft rejection, is reviewed in chapter 1 to present the extent of the problem. Chapter 2 then reviews the mechanisms of allograft rejection from the literature of transplantation immunology, much of which has arisen from studies of kidney, heart, pancreatic islets and liver in animal models. The materials and methods are described in detail in chapter 3, and only the relevant experimental design is detailed in the Materials and Methods sections of the succeeding chapters. The experimental mouse model of transplanting corneal tissue into the renal subcapsular is evaluated in chapter 4, demonstrating that isografts survive indefinitely whereas allografts are rejected typically by 30 days. Pretransplant sensitisation decreased allograft survival time to 10 days. Immunohistochemistry demonstrated the presence of CD4⁺ and CD8⁺ lymphocytes and macrophages at the rejection site. Heterotopic corneal graft recipients were then treated with various monoclonal antibody regimes. Chapter 5 demonstrates that allograft survival can be increased by either anti-CD4 or anti-CD8 therapy, providing near total depletion of the respective lymphocyte subset is achieved. Xenograft rejection is shown to depend on mainly CD4⁺ lymphocytes in chapter 6, with no benefit being found of depleting the CD8⁺ subset in addition. A mild immunosuppressive effect of anti-Vβ8 monoclonal antibody is demonstrated and discussed in chapter 7. The final chapter discusses these results in the light of recent, related work in other transplant systems, and presents a case for a trial of intracameral pan-T-cell monoclonal antibody treatment.

APA, Harvard, Vancouver, ISO, and other styles

7

Chain, Robert Whatley. "THE ROLE OF DENDRITIC CELLS IN GRAFT REJECTION." Master's thesis, Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/194726.

Full text

Abstract:

Microbiology and Immunology
M.S.
Induction of acquired immunological tolerance is the ultimate goal in transplantation. So far the acceptance of a mismatched graft is achieved through immunosuppression that requires long-term treatment and a variety of methods have been explored to prevent rejection and achieve transplant tolerance in mouse models. There are several factors that contribute to acquired tolerance. Recent studies have focused on the inhibition of costimulatory molecules and TLRs in Dendritic Cells (DCs), as a key to the mechanisms underlying the barrier to tolerance induction. Dendritic cells are the sentinels of the immune system. Immature Dendritic cells, which are characterized by low MHC Class II expression and weak T cell stimulation ability, reside in all organs of the body sampling the environment for antigens to bring back to the lymph nodes for T and B cell tolerization or activation, depending on the presence of danger signals. One of these danger signals is LPS from gram-negative Bacteria that can induce DC maturation by triggering TLR4, a surface PRR that is also stimulated by endogenous danger signals, like HMGB1, released during inflammation and tissue damage. Mature DCs highly express MHC II and costimulatory molecules and are potent T cell stimulators. However, LPS has multiple effects on DCs. Indeed, unpublished results from our lab also show that LPS induces DC cell death in vitro and in vivo. It has also been reported that DCs treated with LPS during their development remained in an immature state and they induced alloantigen-specific anergy of CD4+ T cells in vitro. The effects of the simultaneous exposure of DCs to LPS and endogenous danger signals requires further investigation. Therefore, we developed a mouse skin transplant model to determine the effects of LPS and endogenous danger signals, released during engraftment, on DC functions and the ability to induce rejection vs tolerance in transplantation. We used the spontaneous model of skin rejection of a single minor histocompatibility mismatch, the male-specific H-Y antigen. We performed skin grafts from the tail or ear of female or male C57BL/6 mice onto syngeneic female recipients. We administered 4 treatments of PBS 0.5ml or LPS 0.5ml at 25ug/mouse every other day starting from day 0. We observed that control mice transplanted with male skin completely rejected the graft between 24-34 days, while mice transplanted with male skin and treated with LPS did not show rejection of the graft until an average of 64 days and 50% of did not rejected at all. When we administered a different DC stimulator, the TLR9 ligand CpG, we found on the contrary that it induced acceleration of the graft rejection. To understand the mechanism underlying these results, we studied the DCs in vivo. Upon organ transplantation, DCs migrate out of the graft in the first 3 days. Studying the phenotype of the DCs migrating out of the skin graft, we found a sharp decrease of DCs in the skin graft as early as 48 hours post transplant and the loss of DCs was more severe with treatments of LPS. The analysis of the DCs in the epidermal sheets of the graft showed that mice treated with LPS treatment had strongly decreased numbers of DCs compared to mice injected with either PBS or with CpGs. Moreover, we analyzed the DCs from the graft-draining Lymph Nodes (Brachial and Inguinal), and from Spleen. We found again decreased numbers of DCs in both the Spleens and Lymph Nodes of grafted mice treated with LPS compared to mice injected with either PBS or CpGs. Based on these findings, we hypothesize that one of the mechanisms in which LPS prolongs graft survival is that it decreases the number of DCs leaving the graft to stimulate the immune response. LPS is either killing the DCs or holding them outside of the Lymph Nodes, not allowing for antigen presentation during the first week after transplantation when most of the DAMPS from the surgery and ischemia are released.
Temple University--Theses

APA, Harvard, Vancouver, ISO, and other styles

8

Choi, Chi-wai, and 蔡志維. "Detection of class I-related polypeptide-related sequence A (MICA) and angiotensin II type 1 receptor (AT1R) antibodies in antibody mediated rejection in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206596.

Full text

Abstract:

Background: Rejection is considered as a major barrier to achieve successful transplantation. Non self-human leucocyte antigen (HLA) is a well-known antigenic target for antibodies binding that can result in antibody-mediated rejection (AMR). To reduce risk of rejection in kidney transplant, preventive measures are undertaken, which include HLA-matching between donor and recipient, and in-vitro pre-transplant crossmatch with potential donor cells and recipient sera, furthermore, periodic HLA antibodies monitoring for donor-specific antibodies (DSA) is carried out before and after transplant. Nevertheless, allograft may still fail despite the above measures, which suggests other antigens besides HLA can also contribute to renal rejection. In fact, polymorphic major histocompatibility complex (MHC) class I–related chain A (MICA) antigens and Angiotensin II type 1 receptor (AT1R) antigens have been reported as likely targets in AMR. However, the effect of non-HLA antibodies such as anti-MICA and anti-AT1R antibodies in rejection are not fully defined. This implies there is an imminent need to elucidate the role of non-HLA antibodies in allograft AMR cases which are not mediated by HLA antibodies. Aim: To retrospectively evaluate the occurrence of MICA and AT1R antibodies in 21 clinical AMR cases without detectable HLA antibodies or HLA antibodies that were not target against donor HLA. Methods: Twenty-one cases with suspected non-HLA mediated post-transplant rejection were retrieved. Eplet analysis was utilized to confirm that the detectable HLA-DR antibodies in one of the samples were not cross-reactive towards a donor’s antigen. Sera from 21 non-AMR cases were used as controls. All sera were subjected to MICA antibody and AT1R antibody screening. Identified positive cases were further examined with their pre-transplant sera to assess whether the AT1R and/or MICA antibodies were already pre-formed before transplantation. The sensitization histories of transfusion, pregnancy and previous transplantation were recorded. Results: Nine of twenty-one cases were detected with MICA and/or AT1R antibodies. 7 samples were detected with MICA antibodies while 3 samples were detected with AT1R antibodies. A sample was detected with both MICA and AT1R antibodies. Importantly, the presence of MICA/AT1R antibodies appeared to be strongly associated with rejection caused by non-HLA antigens (p=0.0007). All controlled cases were found to be negative for MICA and AT1R antibodies. Pre-transplant sera of the positive cases were further screened and pre-formed antibodies were detected in 3 of the positive MICA cases, and 1 of the positive AT1R cases. Since no AT1R and MICA genotyping of the donor was carried out previously, it was uncertain that the allograft rejection was induced by the donor specific pre-formed antibodies generated in the pre-transplant sensitization events. Nonetheless, AT1R and MICA antibodies appeared to be induced by the allograft in the remaining 5 cases. Conclusion: Presence of MICA/AT1R antibodies appeared to be associated with the investigated AMR cases without detectable HLA antibodies. Some evidence suggested the production of these non-HLA antibodies could be induced by transfusion sensitization or allograft upon transplantation.
published_or_final_version
Pathology
Master
Master of Medical Sciences

APA, Harvard, Vancouver, ISO, and other styles

9

Toogood, Giles John. "Cytokines in small bowel transplantation : expression during graft rejection." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297078.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Figueiredo, Francisco Carlos D'Amorim de. "Immunopathology of corneal graft rejection in a rat model." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296671.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Graft rejection"

1

G, Gubernatis, ed. Acute rejection of liver grafts. Austin: R.G. Landes, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

1946-, Solez Kim, Racusen Lorraine C. 1948-, and Billingham Margaret E. 1930-, eds. Solid organ transplant rejection: Mechanisms, pathology, and diagnosis. New York: Marcel Dekker, Inc., 1996.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Brough, Stephen James Simon. The routes of sensitization in graft rejection. Birmingham: University of Birmingham, 1989.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Hill, John Clifford. The mechanism and management of corneal graft rejection. Amsterdam: Kugler, 1996.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

1948-, Racusen Lorraine C., Solez Kim 1946-, and Burdick James F. 1941-, eds. Kidney transplant rejection: Diagnosis and treatment. 3rd ed. New York: M. Dekker, 1998.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

6

1941-, Burdick James F., ed. Kidney transplant rejection: Diagnosis and treatment. 2nd ed. New York: Dekker, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

7

Conference on Transplantation and Clinical Immunology (28th 1996). Late graft loss: Proceedings of the 28th Conference on Transplantation and Clinical Immunology, 3-5 June, 1996. Dordrecht: Kluwer Academic Publishers, 1997.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

8

1949-, Orosz Charles G., Sedmak Daniel D, and Ferguson Ronald M, eds. Transplant vascular sclerosis. Austin: R.G. Landes, 1995.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

Green, Colin. Recent progress in organ transplantation. Oxford: Medicine Group for the Medicine Publishing Foundation, 1988.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

10

1926-, Starzl Thomas E., and Thomson Angus W, eds. Immunosuppressive drugs: Developments in anti-rejection therapy. London: Edward Arnold, 1994.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Graft rejection"

1

Puri, Sidharth. "Endothelial Graft Rejection." In Encyclopedia of Ophthalmology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_792-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Eslampoor, Alireza. "Subepithelial Graft Rejection." In Encyclopedia of Ophthalmology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_833-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Jee, Kathleen. "Stromal Graft Rejection." In Encyclopedia of Ophthalmology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_911-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Puri, Sidharth. "Endothelial Graft Rejection." In Encyclopedia of Ophthalmology, 724–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_792.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Eslampoor, Alireza. "Subepithelial Graft Rejection." In Encyclopedia of Ophthalmology, 1697–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_833.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Jee, Kathleen. "Stromal Graft Rejection." In Encyclopedia of Ophthalmology, 1689–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_911.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Fogla, Rajesh, and Deepak Soni. "Acute Graft Rejection." In Corneal Emergencies, 259–74. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5876-1_12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Qureshi, Saima M., and Robert A. Copeland. "Corneal Graft Rejection." In Mastering Corneal Surgery, 109–17. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003525004-12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Sibley, Richard K. "Histopathology of chronic rejection." In Late Graft Loss, 13–23. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5434-5_2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Paul, Leendert C., Jagadeesan Muralidharan, Syed A. Muzaffar, and Jean-François Valentin. "Immunological mechanism of chronic rejection." In Late Graft Loss, 51–61. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5434-5_6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Graft rejection"

1

Ma, J., M. J. Smietana, E. M. Wojtys, L. M. Larkin, and E. M. Arruda. "Mechanical Characteristics of Tissue Engineered Bone-Ligament-Bone Constructs Following ACL Replacement in Sheep." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53855.

Full text

Abstract:

With approximately 400,000 reported each year, anterior crucial ligament (ACL) injuries are the most common injury in the US. Unfortunately current ACL replacement strategies, which involve using either allografts from cadavers or autografts from patients’ own patellar tendons (PT) or hamstring tendons as a replacement, have several limitations including graft availability, risk of rejection, increased morbidity and, more importantly, unmatched intra-articular biomechanical properties of grafts and ACL. The objective of this study is to use self-assembling, scaffold-less bone-ligament-bone (BLB) engineered tissue constructs as grafts in a sheep ACL repair model to characterize the biomechanical behaviors of native ACL, PT, and tissue engineered ligament and subsequently present a viable option of using tissue engineered ligament graft for ACL repair.

APA, Harvard, Vancouver, ISO, and other styles

2

Jawaid, Y., A. Caban, F. Jo-Hoy, F. Mora, H. Abdelsalam, J. M. Oropello, A. Bassily-Marcus, and R. Kohli-Seth. "ARDS Associated with Acute Graft Rejection Post Small Bowel Transplant." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7013.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Palma, C. F., R. Katragadda, K. Lee, and M. Fain. "Exudative Urinothorax in a Renal Transplant Patient With Graft Rejection." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a1920.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Huser, B., B. Lämmle, T. H. Tran, M. J. Mihatsch, G. Thiel, and F. Duckert. "FACTOR VIII:C (F VIII:C) AND VON WILLEBRAND FACTOR ANTIGEN (vWFag) IN RENAL TRANSPLANT RECIPIENTS IMMUNOSUPPRESSED WITH CYCLOSPORIN A (CyA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644124.

Full text

Abstract:

In 17 consecutive cadaveric kidney transplant recipients F VIII:C and vWFag were repeatedly determined before transplantation and during 4 months thereafter. Graft biopsy was performed in 12 patients for deterioration of renal function. F VIII:C was determined by a one stage clotting assay using F VIII:C deficient substrate plasma. vWFag was assayed by electroimmunoassay using specific rabbit anti-human vWFag antibodies. Results of F VIII:C and vWFag are expressed referring to NHP as 100%.Results: 2/17 patients lost their graft due to irreversible vascular rejection, 2/17 patients had reversible vascular rejection, 2/17 patients developped glomerulonephritis, 6/17 patients showed acute or chronic CyA nephrotoxicity. In 5/17 patients graft biopsy was not necessary. Despite normalisation of renal function (serum creatinine levels<150umol/L) in 9 out of 17 patients F VIII:C (239 ± 66% to 408 ± 74%, mean ± SD) remained elevated in all 17 patients. vWFag (181 ± 29% to 454 ± 84%) was normalised in only 2 out of 17 patients. CyA dosis and CyA blood levels were not correlated with F VIII:C and vWFag. All 4 patients with histological vascular rejection, both patients with later developping glomerulonephritis and 3 out of 6 patients with later developping CyA nephrotoxicity showed F VIII:C/vWFag quotients > 1 (1,1 to 1,3) Four out of 5 patients with well functioning graft had F VIII:C/ vWFag quotients consistently <1 (0,68 to 0,92).Conclusion: 1. The elevated F VIII:C and vWFag levels in chronic renal failure are not normalised during 4 months of observation despite normalisation of renal function by transplantation and immunosuppression with CyA.2. A quotient F VIII :C/vWFag < 1 may indicate a good prognosis for kidney allograft function in the absence of CyA nephrotoxicity whereas later developping graft rejection or glomerulonephritis were associated with F VIII:C/vWFag>1.

APA, Harvard, Vancouver, ISO, and other styles

5

Hegde, Satyanarayan, Binal Kancherla, Leah Hennings, and Okan Elidemir. "Angiopoietin-2 Expression Is Increased In Graft Tissues In Lung Transplant Rejection." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2566.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Daccarett-Bojanini, W. N., R. Wang, S. Yegnasubramanian, N. M. Heller, and J. M. Dodd-o. "Decitabine Affects Lung Monocyte-macrophage Dynamics and Phenotype in Acute Lung Graft Rejection." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4973.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Salaam, Amanee D., and Derrick Dean. "Electrospun Polycaprolactone-Nanodiamond Composite Scaffolds for Bone Tissue Engineering." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13298.

Full text

Abstract:

Every year, there are roughly 8 million bone fractures in United States [1]. In addition, approximately 2300 new cases of primary bone cancer are diagnosed each year [2]. Yet, the number of people suffering from bone disease is significantly greater; about 10 million people in the U.S. alone suffer from osteoporosis [3]. Consequently, surgeons perform nearly 500,000 bone graft operations annually making bone grafts the second most frequently transplanted materials [4]. Although there is an extremely high demand for treatment of bone abnormalities, the current grafting methods fail to meet these demands due to several limitations. Autografting has the fewest problems with rejection and pathogen transmission, however in some cases the availability may be limited or not be possible (e.g., genetic diseases). With other methods of transplantation such as allogafting and xenografting where tissue is acquired from other humans or species, respectively, the receptor’s immune system causes an increased risk of chronic rejection [5]. Notably, the major drawback with all these methods is that they often require multiple painful and invasive surgeries.

APA, Harvard, Vancouver, ISO, and other styles

8

Fisher, M. S., A. S. Bulygin, V. V. Kurilin, Yu N. Khantakova, and S. V. Sennikov. "INDUCTION OF ANTIGEN-SPECIFIC IMMUNOLOGICAL TOLERANCE BY REGULATORY T-CELLS IN COLLAGEN-INDUCED ARTHRITIS AND TRANSPLANTATION, IN VITRO." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-383.

Full text

Abstract:

Induction of antigen-specific immunological tolerance with CD25 high FoxP3 hi T-regulatory cells (T-reg), plays an important role in organ transplant rejection, graft-versus-host disease, and autoimmune diseases, and helps to reduce the severity and incidence of adverse reactions associated with systemic immunosuppression in the use of traditional therapy

APA, Harvard, Vancouver, ISO, and other styles

9

Bulygin, A. S., M. S. Fisher, V. V. Kurilin, Yu N. Khantakova, and C. V. Sennikov. "INDUCTION OF IMMUNOLOGICAL TOLERANCE TO GRAFT ALLOANTIGENS IN SKIN FLAP MODEL USING TRANSFECTED DENDRITIC CELLS AND AN INHIBITOR OF CYCLIN-DEPENDENT KINASES 8/19." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-302.

Full text

Abstract:

The induction of transplantation tolerance through the induction of donor-specific T cells with tolerogenic DCs and ar-Tregs may provide additional opportunities to overcome the problem of organ rejection during transplantation. With the introduction of DC transfected with DNA constructs and anti-Treg obtained by stimulation with AS2863619, the prolongation of the rejection of the transplanted skin flap increased compared to the control group.

APA, Harvard, Vancouver, ISO, and other styles

10

Joseph, Naomi, Beth Ann Benetz, Harry Menegay, Silke Oellerich, Lamis Baydoun, Gerrit Melles, Jonathan Lass, and David L. Wilson. "Early detection of at-risk keratoplasties and prediction of future corneal graft rejection from pre-diagnosis endothelial cell images." In Computer-Aided Diagnosis, edited by Karen Drukker and Maciej A. Mazurowski. SPIE, 2021. http://dx.doi.org/10.1117/12.2582171.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Graft rejection"

1

Pelletier, Joseph P., Oluwole Fadare, and Yanyun Wu. Post-Renal Transplant Thrombotic Thrombocytopenic Purpura (TTP): Attributable to Immunosuppression or Graft Rejection? Report of Three Cases and Literature Review. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada429608.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!