Academic literature on the topic 'Donor-specific antiboy'
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Journal articles on the topic "Donor-specific antiboy"
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Tinckam, Kathryn J., and Peter S. Heeger. "Complementing donor-specific antibody testing." Nature Reviews Nephrology 9, no. 12 (November 5, 2013): 713–14. http://dx.doi.org/10.1038/nrneph.2013.234.
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Mcmillan, M. A., J. D. Briggs, B. J. R. Junor, R. N. M. Macsween, and G. P. Sandilands. "DONOR-SPECIFIC TRANSFUSION AND ANTIBODY RESPONSE." Lancet 329, no. 8535 (March 1987): 744–45. http://dx.doi.org/10.1016/s0140-6736(87)90382-5.
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Book, B. K., N. G. Higgins, G. J. Eckert, K. M. Rosner, A. Lobashevsky, and M. D. Pescovitz. "DONOR SPECIFIC ANTIBODY CHANGES AFTER NEPHRECTOMY." Transplantation Journal 90 (July 2010): 378. http://dx.doi.org/10.1097/00007890-201007272-00697.
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Zhang, Rubin. "Donor-Specific Antibodies in Kidney Transplant Recipients." Clinical Journal of the American Society of Nephrology 13, no. 1 (April 26, 2017): 182–92. http://dx.doi.org/10.2215/cjn.00700117.
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Donor-specific antibodies have become an established biomarker predicting antibody-mediated rejection. Antibody-mediated rejection is the leading cause of graft loss after kidney transplant. There are several phenotypes of antibody-mediated rejection along post-transplant course that are determined by the timing and extent of humoral response and the various characteristics of donor-specific antibodies, such as antigen classes, specificity, antibody strength, IgG subclasses, and complement binding capacity. Preformed donor-specific antibodies in sensitized patients can trigger hyperacute rejection, accelerated acute rejection, and early acute antibody-mediated rejection. De novo donor-specific antibodies are associated with late acute antibody-mediated rejection, chronic antibody-mediated rejection, and transplant glomerulopathy. The pathogeneses of antibody-mediated rejection include not only complement-dependent cytotoxicity, but also complement-independent pathways of antibody-mediated cellular cytotoxicity and direct endothelial activation and proliferation. The novel assay for complement binding capacity has improved our ability to predict antibody-mediated rejection phenotypes. C1q binding donor-specific antibodies are closely associated with acute antibody-mediated rejection, more severe graft injuries, and early graft failure, whereas C1q nonbinding donor-specific antibodies correlate with subclinical or chronic antibody-mediated rejection and late graft loss. IgG subclasses have various abilities to activate complement and recruit effector cells through the Fc receptor. Complement binding IgG3 donor-specific antibodies are frequently associated with acute antibody-mediated rejection and severe graft injury, whereas noncomplement binding IgG4 donor-specific antibodies are more correlated with subclinical or chronic antibody-mediated rejection and transplant glomerulopathy. Our in-depth knowledge of complex characteristics of donor-specific antibodies can stratify the patient’s immunologic risk, can predict distinct phenotypes of antibody-mediated rejection, and hopefully, will guide our clinical practice to improve the transplant outcomes.
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Habig, Dennis F., Justine L. Gaspari, Parvez M. Lokhandwala, Ronald E. Domen, Catherine S. Abendroth, Zakiyah Kadry, Nasrollah Ghahramani, Riaz Ali Shah, Ashokkumar Jain, and Hiroko Shike. "Donor-specific antibody to trans-encoded donor HLA-DQ heterodimer." Human Immunology 76, no. 8 (August 2015): 587–90. http://dx.doi.org/10.1016/j.humimm.2015.09.004.
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Everly, M. J., J. J. Everly, B. Susskind, P. Brailey, L. J. Arend, R. R. Alloway, P. Roy-Chaudhury, et al. "Proteasome Inhibition Reduces Donor-Specific Antibody Levels." Transplantation Proceedings 41, no. 1 (January 2009): 105–7. http://dx.doi.org/10.1016/j.transproceed.2008.10.073.
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Matsumoto, Cal, Jason Hawksworth, Alexander H. Kroemer, Raffaele GIrlanda, Nada Yazgi, Khalid Khan, Stuart S. Kaufman, et al. "Denovo Donor Specific Antibody in Intestinal Transplantation." Transplantation 101 (June 2017): S5. http://dx.doi.org/10.1097/01.tp.0000521279.38245.2d.
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Hawksworth, Jason S., and Cal S. Matsumoto. "Donor-specific antibody management in intestine transplantation." Current Opinion in Organ Transplantation 24, no. 2 (April 2019): 212–18. http://dx.doi.org/10.1097/mot.0000000000000619.
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Schwaiger, Elisabeth, Farsad Eskandary, Nicolas Kozakowski, Gregor Bond, Željko Kikić, Daniel Yoo, Susanne Rasoul-Rockenschaub, Rainer Oberbauer, and Georg A. Böhmig. "Deceased donor kidney transplantation across donor-specific antibody barriers: predictors of antibody-mediated rejection." Nephrology Dialysis Transplantation 31, no. 8 (March 24, 2016): 1342–51. http://dx.doi.org/10.1093/ndt/gfw027.
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Ma, Jeffrey, Anita Patel, and Kathryn Tinckam. "Donor-Specific Antibody Monitoring: Where Is the Beef?" Advances in Chronic Kidney Disease 23, no. 5 (September 2016): 317–25. http://dx.doi.org/10.1053/j.ackd.2016.08.004.
Full textDissertations / Theses on the topic "Donor-specific antiboy"
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Chen, Chien-Chia. "Réponse humorale alloimmune après greffe d’îlots pancréatiques : caractéristiques et impact sur la fonction du greffon." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1040.
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Le diabète de type 1 est une maladie auto-immune chronique fréquente au cours l'enfance qui résulte de la destruction des cellules ß des îlots de Langerhans produisant l'insuline (seule hormone régulant la glycémie).Contrairement à l'administration d'insuline exogène, la greffe d'îlots pancréatiques restaure une production endogène d'insuline et prévient ainsi plus efficacement la morbi-mortalité résultant du diabète.Malheureusement, la fonction des îlots greffés diminue avec le temps du fait de la réponse alloimmune qui se développe contre les molécules HLA spécifiques du donneur. Le système immunitaire adaptatif du receveur peut détruire les îlots allogéniques par deux mécanismes: le rejet cellulaire impliquant les lymphocytes T cytotoxiques et le rejet humoral (RH) impliquant les anticorps anti-donneur (ASD).Alors qu'en transplantation d'organe, le RH est reconnu comme la principale cause de perte des organes, son rôle dans la greffe d'îlots est encore mal défini.Notre objectif est de: i) caractériser la réponse humorale allo-spécifique après greffe d'îlots, et ii) déterminer l'impact des ASD sur la fonction du greffon.Notre travail confirme que la greffe d'îlots est un évènement immunisant pour les receveurs. Le risque de développer des ASD augmente après réduction/arrêt des immunosuppresseurs. Cependant, à l'inverse de la transplantation d'organe, les ASD n'ont pas d'effet délétère sur la survie du greffon en clinique. En utilisant des modèles murins, nous démontrons que les îlots allogéniques sont résistants au RH alors que les ASD peuvent détruire les cellules ß in vitro. Cette résistance au RH s'explique par la combinaison i) d'une séquestration vasculaire des ASD, qui ne peuvent pas accéder aux cellules ß allogéniques in vivo et ii) le fait que contrairement à la vascularisation des organes transplantés qui provient du donneur, celle des îlots greffés provient du receveurType 1 diabetes, the most prevalent chronic diseases of childhood, is caused by an autoimmune-mediated destruction of pancreatic insulin-producing ß cells, the unique cells responsible for glucose level regulation.In contrast to exogenous insulin administration, pancreatic islet grafting restores endogenous secretion, which more efficiently prevents secondary end-organ complications and life-threatening events.Unfortunately, islet graft function decreases over time due to alloimmune response that developed against donor-specific HLA molecules. Recipient’s adaptive immune system can destroy allogeneic islets through two distinct mechanisms: cellular rejection by cytotoxic T-cells and antibody-mediated rejection (AMR). Donor-specific anti-HLA antibodies (DSA) are increasingly recognized as the prime cause of solid organ transplant failure, but the impact of the humoral alloimmune response of recipient on islet graft remains ill defined.Our thesis aimed at: i) characterizing the humoral alloimmune response of islet graft recipients, and ii) determining the impact of DSA on islet graft.Our work confirms that islet grafting is an HLA sensitizing event for recipients. The risk of DSA generation increases with the reduction/discontinuation of immunosuppressive drugs. However, in contrast with solid organ transplantation, DSA did not negatively impact graft survival in the clinic. Using a combination of murine models, we demonstrate that allogeneic islets are indeed resistant to AMR despite the fact that DSA can destroy islet cells in vitro. The resistance of allogeneic islets to AMR is explained by the combination of i) vascular sequestration of DSA, which are unable to access the allogeneic ß cells in vivo and ii) the fact that unlike vascularization of transplanted organs (that comes from the donor), islet graft vascularization develops from the recipient
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Wiebe, Chris. "De novo donor-specific antibodies in renal transplantation." Wiley Periodicals Inc, 2012. http://hdl.handle.net/1993/23678.
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The natural history for patients with de novo donor-specific antibodies (dnDSA) and the risk factors for its development have not been well defined. Furthermore, clinical and histologic correlation with serologic data is limited. We studied 315 consecutive renal transplants without pre-transplant donor-specific antibody (DSA), with a mean follow-up of 6.2 ± 2.9 years. Protocol (n = 215) and for cause (n = 163) biopsies were analyzed. Solid phase assays were used to screen for dnDSA post-transplant. A total of 47 out of 315 (15%) patients developed dnDSA at a mean of 4.6 ± 3.0 years post-transplant. Independent predictors of dnDSA were HLA-DRβ1 MM > 0 (OR 5.66, p < 0.006); and non-adherence (OR 8.75, p < 0.001); with a strong trend toward clinical rejection episodes preceding dnDSA (OR 1.57 per rejection episode, p=0.061). The median 10-year graft survival for those with dnDSA was lower than the No dnDSA group (57% vs. 96%, p < 0.0001).
Pathology consistent with antibody-mediated injury occurred and progressed in patients with dnDSA in the absence of graft dysfunction. Furthermore, non-adherence and cellular rejection contributed to both dnDSA development and the risk of progression to graft loss.
(Human leukocyte antigen) HLA epitope matching is a novel strategy that may minimize dnDSA development. HLAMatchmaker software was used to characterize epitope mismatches at 395 potential HLA-DR/DQ/DP conformational epitopes for a subset of 286 donor–recipient pairs in which samples were available for high-resolution HLA-typing. Epitope specificities were assigned using single antigen HLA bead analysis and correlated with known monoclonal alloantibody epitope targets. Locus-specific epitope mismatches were more numerous in patients who developed HLA-DR dnDSA alone (21.4 vs. 13.2, p<0.02) or HLA-DQ dnDSA alone (27.5 vs. 17.3, p<0.001). An optimal threshold for epitope mismatch (10 for HLA-DR, 17 for HLA-DQ) was defined that was associated with minimal development of Class II dnDSA using a receiver operating characteristic analysis. Applying these thresholds, 0% and 2.7% of patients developed dnDSA against HLA-DR and HLA-DQ, respectively, after a median of 6.9 years follow-up. Epitope specificity analysis revealed that 3 HLA-DR and 3 HLA-DQ epitopes were independent multivariate predictors of Class II dnDSA when mismatched between the donor and recipient.
HLA-DR and DQ epitope matching outperforms traditional low-resolution antigen-based matching and has the potential to minimize the risk of de novo Class II DSA development, thereby improving long-term graft outcome.
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Hamer, Rizwan. "Donor specific antibodies and the complement system in HLA-antibody incompatible renal transplantation." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/51636/.
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Despite advances in medical science, dialysis treatment for end stage renal disease remains fraught with complications and severely limits the quality and longevity of life in these patients. Renal transplantation allows for an enhanced length and quality of life. Unfortunately the demand for kidneys outstrips the supply and nephrologists have taken to performing transplantation in conditions that were previously thought impossible. Human leucocyte antigen (HLA) antibody incompatible transplantation, a process of transplanting kidneys into recipients who have antibodies against HLA antigen on the donor kidney, has recently become an acceptable mode of transplanting patients who would have previously died whilst on dialysis. Although increasingly successful, the Achilles’ heel of this form of transplantation remains acute antibody mediated rejection (AMR), a particularly severe form of rejection. It is generally accepted that the complement system is intricately involved in the process of acute AMR and, indeed, C4d, a split product of complement factor C4, when detected on renal biopsies in the correct context, is considered by the BANFF classification (an internationally accepted method of classifying renal transplant rejection) to be a hallmark feature of acute AMR. The sensitivity and specificity of this test, however, is increasingly debated and requires an interventional diagnostic test that is not without risk. A “blood” test to detect or predict the onset of acute AMR is not available. In addition, although the complement system is known to be involved in acute AMR, characterisation of the three complement pathways and the degree of their systemic activation has not been fully described. Although the liver is the main source of complement factors in the body, other organs such as the kidney, are capable of synthesizing complement. It is unknown whether the complement factors involved in acute AMR following renal transplantation are of systemic or local origin. It is also not known which renal cell, if any, is responsible for this. Importantly, the first cells to encounter antibodies against antigen on their surfaces, the renal microvascular endothelial cells, have not so far been shown to be able to produce complement factors. This thesis briefly examines changes in antibody levels during the process of HLA antibody incompatible transplantation, histological features associated with subsequent graft dysfunction and possible serum markers (soluble CD27 and Cd30) that could indicate onset of AMR. Whilst anti-HLA antibody monitoring was found to be useful in the management of patients it was not possible to use levels to predict rejection or accommodation of the graft. No correlation was found between soluble factors CD27 and CD30 and AMR. The thesis then examines the effect of HLA antibody incompatible renal transplantation on the complement pathways and on the levels of complement factors C3a and C4a. There was no systemic pathway activation in the presence of rejection. Systemic levels of C3a and C4a did not rise with a simultaneous increased level of HLA antibodies or with rejection episodes. Indeed, in patients who did not have an episode of rejection and in those with rejection but no evidence of C4d on renal biopsy, mean C4a levels were significantly lower at 4-6 weeks when compared to those who did have C4d-postive AMR. This points to a role for inhibitory mechanisms in these patients. The thesis also demonstrates the ability of microvascular endothelial cells (including of glomerular origin for the first time) to produce complement C4 on stimulation with gamma interferon and with antibodies against the cell HLA type. Finally, the thesis briefly examines the possible use of a complement inhibitor in the treatment of AMR.
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Hirata, Yoshihiro. "Impact of Antibodies that React with Liver Tissue and Donor-specific anti-HLA Antibodies in Pediatric Idiopathic Posttransplantation Hepatitis." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225483.
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Yoshizawa, Atsushi. "Significance of Semiquantitative Assessment of Preformed Donor-Specific Antibody Using Luminex Single Bead Assay in Living Related Liver Transplantation." Kyoto University, 2013. http://hdl.handle.net/2433/180459.
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Matia, Ivan, Peter Fellmer, Katrin Splith, Martin Varga, Milos Adamec, Ines Kämmerer, Linda Feldbrügge, et al. "Immunosuppressive protocol with delayed use of low-dose tacrolimus after aortic transplantation suppresses donor-specific anti-MHC class I and class II antibody production in rats." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-167365.
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Background: Arterial allografts are used as vascular conduits in the treatment of prosthetic graft infection. Immunosuppression
decreases their rupture risk rate. However, immunosuppression can be unprofitable in florid infection. Previously, we confirmed inhibition of cell-mediated destruction of rat aortic grafts by delayed use of tacrolimus. In this work, we studied the influence of this protocol on the antibody-mediated rejection.
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Sadaka, Basma. "Differences in histologic response between early and late antibody mediated rejection therapy: assessment by Banff component scoring." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367925543.
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Glasberg, Denise Segenreich. "Monitorização dos anticorpos anti-hla após transplante renal e sua correlação com episódios de rejeição aguda." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=7473.
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Introdução: A associação entre a presença de anticorpo anti-HLA doador específico (DSA), em pacientes com prova cruzada negativa por citotoxicidade dependente de complemento (CDC), e a ocorrência de episódios de rejeição mediada por anticorpos (RMA) e menor sobrevida do enxerto já foi demonstrada por diversos autores. Entretanto,estimar a relevância clínica da presença desses anticorpos, em um determinado receptor, é um grande desafio e portanto novas estratégias de monitorização imunológicas são necessárias. Objetivo: O objetivo desse estudo foi monitorar a presença de DSA, bem como a variação dos seus títulos durante o primeiro ano após o transplante renal e correlacionar com episódios de rejeição aguda e função do enxerto ao final desse período. Metodologia: Foram analisados 389 soros de 71 pacientes incluídos no estudo. A pesquisa de DSA foi realizada utilizando os testes LABScreen single antigenbeads nas amostras correspondentes aos tempos: pré-transplante, 14, 30, 90, 180 e 365 dias após o transplante. Episódios de rejeição aguda comprovados por biópsia foram analisados de acordo com a classificação de Banff 2007. A taxa de filtração glomerular (TFG) ao final do primeiro ano foi estimada utilizando a fórmula Modificationof Diet in Renal Disease (MDRD). Os pacientes foram inicialmente separados em 3 grupos de diferentes riscos imunológicos (pré-transplante): A) DSA-, B) DSA+ com MFI >1000 e < 5000 e C) DSA+ com MFI > 5000. Num segundo momento, foram novamente agrupados de acordo com o perfil de mudança nos valores de MFI (intensidade de fluorescência média) ao longo do primeiro ano. Resultados: DSA estavam presentes pré-transplante em 15 pacientes. RMA foi mais frequente no grupo C (p = 0,02). De acordo com a variação dos títulos de DSA pós-transplante os pacientes foram novamente agrupados: grupo I) permaneceu DSA- durante todo acompanhamento = 50 pacientes, II) diminuiu ou manteve títulos de DSA em relação ao tempo zero = 13 pacientes e III) aumentou títulos em relação ao tempo zero = 8 pacientes (6 foram DSA de novo). Três pacientes dos grupos I e um paciente do grupo II apresentaram episódios de rejeição aguda celular. Não foi observada oscilação significativa nos títulos de anticorpos durante esses eventos. Nenhum paciente desse grupo apresentou episódio de RMA. Episódio de RMA ocorreu em dois pacientes do grupo III. Em ambos os pacientes foi detectado aumento significativo nos valores de MFI dos DSA em relação ao tempo zero. Não foi observada diferença significativa na TFG entre os grupos analisados nesse estudo. Entretanto, observou-se uma diferença estatisticamente significativa na TFG entre os pacientes que apresentaram episódio de rejeição aguda em relação aos que não tiveram, sendo menor nos primeiros (p = 0,04). Conclusão: A monitorização prospectiva dos anticorpos pode ajudar a identificar pacientes em maior risco para ocorrência de RMA e o aumento nos valores de MFI DSA deve ser interpretado como um sinal de alerta, sobretudo em pacientes previamente sensibilizados.Introdução: A associação entre a presença de anticorpo anti-HLA doador específico (DSA), em pacientes com prova cruzada negativa por citotoxicidade dependente de complemento (CDC), e a ocorrência de episódios de rejeição mediada por anticorpos (RMA) e menor sobrevida do enxerto já foi demonstrada por diversos autores. Entretanto,estimar a relevância clínica da presença desses anticorpos, em um determinado receptor, é um grande desafio e portanto novas estratégias de monitorização imunológicas são necessárias. Objetivo: O objetivo desse estudo foi monitorar a presença de DSA, bem como a variação dos seus títulos durante o primeiro ano após o transplante renal e correlacionar com episódios de rejeição aguda e função do enxerto ao final desse período. Metodologia: Foram analisados 389 soros de 71 pacientes incluídos no estudo. A pesquisa de DSA foi realizada utilizando os testes LABScreen single antigenbeads nas amostras correspondentes aos tempos: pré-transplante, 14, 30, 90, 180 e 365 dias após o transplante. Episódios de rejeição aguda comprovados por biópsia foram analisados de acordo com a classificação de Banff 2007. A taxa de filtração glomerular (TFG) ao final do primeiro ano foi estimada utilizando a fórmula Modificationof Diet in Renal Disease (MDRD). Os pacientes foram inicialmente separados em 3 grupos de diferentes riscos imunológicos (pré-transplante): A) DSA-, B) DSA+ com MFI >1000 e < 5000 e C) DSA+ com MFI > 5000. Num segundo momento, foram novamente agrupados de acordo com o perfil de mudança nos valores de MFI (intensidade de fluorescência média) ao longo do primeiro ano. Resultados: DSA estavam presentes pré-transplante em 15 pacientes. RMA foi mais frequente no grupo C (p = 0,02). De acordo com a variação dos títulos de DSA pós-transplante os pacientes foram novamente agrupados: grupo I) permaneceu DSA- durante todo acompanhamento = 50 pacientes, II) diminuiu ou manteve títulos de DSA em relação ao tempo zero = 13 pacientes e III) aumentou títulos em relação ao tempo zero = 8 pacientes (6 foram DSA de novo). Três pacientes dos grupos I e um paciente do grupo II apresentaram episódios de rejeição aguda celular. Não foi observada oscilação significativa nos títulos de anticorpos durante esses eventos. Nenhum paciente desse grupo apresentou episódio de RMA. Episódio de RMA ocorreu em dois pacientes do grupo III. Em ambos os pacientes foi detectado aumento significativo nos valores de MFI dos DSA em relação ao tempo zero. Não foi observada diferença significativa na TFG entre os grupos analisados nesse estudo. Entretanto, observou-se uma diferença estatisticamente significativa na TFG entre os pacientes que apresentaram episódio de rejeição aguda em relação aos que não tiveram, sendo menor nos primeiros (p = 0,04). Conclusão: A monitorização prospectiva dos anticorpos pode ajudar a identificar pacientes em maior risco para ocorrência de RMA e o aumento nos valores de MFI DSA deve ser interpretado como um sinal de alerta, sobretudo em pacientes previamente sensibilizados.
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Miyamoto, Ei. "Association of Local Intrapulmonary Production of Antibodies Specific to Donor Major Histocompatibility Complex Class I With the Progression of Chronic Rejection of Lung Allografts." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263561.
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Redondo, Pachón Dolores. "Monitorización sérica e histológica del rechazo mediado por anticuerpos en trasplante renal." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/650402.
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El trasplante renal es el tratamiento de elección en los pacientes con enfermedad renal crónica avanzada porque mejora la supervivencia del paciente, su calidad de vida e implica menores costes si lo comparamos con el tratamiento sustitutivo mediante diálisis. En los últimos años, los avances en la inmunosupresión, la mejora en las técnicas quirúrgicas y el mejor conocimiento de la inmunología del trasplante han permitido incrementar la supervivencia del paciente y del injerto a corto plazo, con menor impacto en las tasas de pérdida a medio y largo plazo. Se han producido dos importantes avances en la última década: el desarrollo de nuevas técnicas de detección de anticuerpos frente a antígenos HLA y la caracterización histológica del rechazo mediado por anticuerpos.
El objetivo de la presente tesis ha sido profundizar en el conocimiento del rechazo mediado por anticuerpos abordando nuevos aspectos desde estos dos puntos de vista: estudio serológico de los anticuerpos HLA y caracterización histológica del rechazo humoral.
Para ello, hemos analizado una amplia cohorte de pacientes trasplantados con estudio de anticuerpos antiHLA pre y postrasplante determinados mediante tecnología Luminex. Los pacientes con anticuerpos dirigidos frente al donante detectados pretrasplante presentan una peor supervivencia del injerto y mayor riesgo de rechazo mediado por anticuerpos; y este riesgo sigue incrementado tanto si persiste como si no persiste el anticuerpo después del trasplante o aparece de novo. Por otro lado, hemos realizado el estudio de otros anticuerpos considerados clásicamente menos inmunogénicos y con poca relevancia en el campo del trasplante hasta la fecha, pero que las nuevas técnicas en fase sólida permiten identificar, como son los anticuerpos frente a los antígenos HLA DP. En nuestra experiencia, el 10% de los pacientes trasplantados presentan anticuerpos antiHLA-DP detectados por Luminex, tanto pre como postrasplante. La presencia de estos anticuerpos no parece modificar el impacto en la supervivencia del injerto.
Desde el punto de vista histológico, hemos demostrado que el rechazo mediado por anticuerpos es un diagnóstico frecuente en las biopsias tardías de injerto renal realizadas por indicación según los criterios de la clasificación de Banff 2013, y confiere un peor pronóstico que otras categorías histológicas. Finalmente, hemos profundizado en el análisis de la categoría histológica de rechazo mediado por anticuerpos comparando la clasificación de Banff 2009 con la nueva definición de cambios mediados por anticuerpos de la clasificación de Banff 2013. Según nuestros resultados, la clasificación de Banff 2013 proporciona un diagnóstico más preciso del rechazo mediado por anticuerpos.Kidney transplantation is considered the treatment of choice for patients with end-stage renal disease. It is associated with improved survival, better quality of life and reduced costs when compared with dialysis. Throughout the years, the progress in immunosuppression, the improvement in surgical techniques and a better understanding of transplant immunology have produced an increase in both patient and graft survival short-term, notwithstanding in medium and long-term outcomes. Two major developments have taken place over the last decade: the development of new techniques to detect HLA antibodies, and the histological characterization of antibody-mediated rejection. The aim of this thesis has been to expand the knowledge of antibody-mediated rejection by addressing the issue from these two points of view: HLA antibody serological testing with new techniques and histological characterization of humoral rejection. To that end, we have analyzed a large cohort of transplant patients with pre and post-transplant anti-HLA antibodies determined by Luminex technologies. Patients with preformed donor specific antibodies show worse graft survival and greater risk of antibody-mediated rejection, regardless potential DSA clearing after transplantation. Furthermore, we evaluated the impact of typically less immunogenic antibodies believed to be less relevant in the transplant field thus far, such as HLA DP antibodies, albeit detectable by newer solid phase techniques. In our experience, 10% of transplant patients show HLA DP antibodies as detected by Luminex assay both pre and post-transplant. The presence of these antibodies does not seem to modify graft survival Histologically, we have shown that antibody-mediated rejection is a common diagnosis most often seen in late kidney graft biopsies according to the Banff 2013 classification criteria; antibody-mediated rejection also shows worse prognosis compared to other histological categories. Eventually, we have delved into the analysis of the antibody-mediated rejection category by comparing the Banff 2009 classification to the new antibody-mediated changes from Banff 2013. According to our results, Banff 2013 classification provides a more accurate diagnosis of antibody-mediated rejection.
Book chapters on the topic "Donor-specific antiboy"
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Lazarovits, A. I., and R. Z. Zhong. "Renal Allografts in the Mouse and Donor-Specific Tolerance Induced by Antibody to CD45RB." In Organtransplantation in Rats and Mice, 653–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_67.
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Watanabe, Takuya, and Norihide Fukushima. "Novel Diagnostic and Therapeutic Approach to Antibody-Mediated Rejections in Heart Transplantation." In Immunosuppression. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93081.
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Despite the improvement of immunosuppressive therapy in heart transplantation (HTx), antibody-mediated rejection (AMR) is still a great obstacle to prolong cardiac graft survival. Anti-donor-specific antibodies (DSAs), especially anti-donor human leukocyte antigen (HLA) antibody, lead to heart graft failure resulting in hemodynamic consequence and often in the recipient death. To prevent hyperacute rejection, prospective complement-dependent cytotoxicity test has been performed in every cardiac donor in Japan. But in other solid organ transplantations, flow cytometry crossmatch has been recently recommended to crossmatch to select the recipient in Japan as well as the world. However, flow cytometry is too sensitive to select the recipient, because not all DSAs determined by flow cytometry are cytotoxic to the cardiac graft. On the first complement classical pathway, alloantibodies bind to HLA antigens on cells of the graft and then recruit C1q, which is essential to make membrane attack complex and kill the cell. We review a role of the novel monitoring method of complement pathway regarding C1q in occurrence of AMR and its diagnostic and therapeutic significance in managing AMR in HTx.
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Campbell, Sean, and Darshana Dadhania. "Monitoring and Management of the Kidney Transplant Recipients with Donor Specific Antibody." In Challenges and Controversies in Kidney Transplantation, 125. Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12525_10.
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Clerkin, Kevin J., and Maryjane A. Farr. "Orthotopic Heart Transplant Rejection and Immunosuppression." In Cardiothoracic Critical Care, 247–56. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190082482.003.0026.
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This chapter focuses on orthotopic heart transplant rejection. Hyperacute rejection is a catastrophic complication that occurs early post-transplantation. This type of rejection is most often due to pre-formed donor-specific anti–human leukocyte antigen antibodies or an ABO blood type mismatch and is rarely seen in the current era because pre-transplant virtual and prospective crossmatch has become routine practice. Meanwhile, immune activation of recipient T cells against the cardiac allograft causes acute cellular rejection (ACR). Treatment of ACR will vary depending on the grade of rejection, symptoms, and hemodynamic significance. On the other hand, antibody-mediated rejection (AMR), previously known as humoral or vascular rejection, is primarily mediated by antibodies and not T cells, as in ACR. AMR is difficult to treat because it may persist or be recurrent and is associated with an increased risk of cardiac allograft vasculopathy and mortality. The chapter then discusses the management of acute rejection. Induction therapy is augmented immunosuppression in the early period following heart transplantation, when the recipient is at the greatest risk of rejection. Maintenance immunosuppression includes calcineurin inhibitors, anti-metabolites, glucocorticoids, and proliferation signal inhibitors.
Conference papers on the topic "Donor-specific antiboy"
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Immohr, M. B., H. Aubin, R. Westenfeld, A. Mehdiani, D. Scheiber, R. Bruno, I. Tudorache, P. Akhyari, A. Lichtenberg, and U. Boeken. "Treatment of Donor-Specific Antibody-Mediated Rejection After Heart Transplantation by IGM-Enriched Human Intravenous Immunoglobulin." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725614.
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von dem Borne, A. E. G. Kr, and W. H. Ouwehand. "ALLOIMMUNIZATION TO PLATELET TRANSFUSIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643997.
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Alloimmunization against platelets is an important cause of refractioness to transfusion of this blood product.It may occur in up to 66% of patients, with malignant blood diseases or aplastic anaemia, whoreceive platelet transfusions for thrombocytopenia.The alloantibodies responsible for refractioness areoften anti-HLA-ABC antibodies, but in about 20% platelet specific allo- antibodies may (also) play a role.In recent years major progress has been made in the methodology of platelet antibody detection. Reliabletechniques to detect platelet antibodies and antigens have been developed, based on the antiglobulin principle. Platelet immunofluorescence is the standard and reference method, but platelet radio-immuno assays and enzyme-linked immuno-assay appear to be good alternatives. A problem is still the quality of the antiglobulin reagents applied, which appears to be often poor.A new development is the study of antibody binding at the level of platelet membrane glycoproteins, instead of intact platelets. This can be done in the immunoblot, but also with chemically purified glycoproteins, or glycoproteins specifically captured by monoclonal antibodies. It gives direct information aboutthe chemical structures involved in the alloimmune response. Most of these methods are still in the investigational stage, but the immunoblot has already found a place in the routine laboratory. A limitation of the immunoblot is that it is quite insensitive and often gives non-specific results.An important question in platelet serology is whether a positive platelet antibody test is due to HLA-antibodies or to platelet specific antibodies. To answer this question, combined tests on platelets and lymphocytes, obtained from the same donor, are usuallyperformed. Complicated studies on cell panels of typed donors, with absorptions and elutions, may often be necessary.However chloroquine treatment of the platelets, which leads to elution of HLA-antigens, isthan a very helpfull new technique, as are techniqueswhich use isolated glycoproteins.Platelet specific antibodies may be directed againsthidden or cryptic antigens of glycoprotein Ilb/IIIa, which are exposed upon alteration of the platelets, for instance by fixation or Na2EDTA.The recognition of such antibodies is important, because they are not responsible for increased platelet destruction and may cause 'falsely 'positive test results.Modern platelet antibody technology has made it possible to perform platelet crossmatching. In refractory patients an obvious first approach is the selection of platelets from cross-match negative random donors. In many patients satisfactory platelets increments can be obtained again in this way. Only in patients with multiple HLA antibodies in the blood, HLA-typing and the transfusion of HLA-compatible donor platelets is than necessary.HLA-alloimmunization occurs much more frequently on blood products that contain leukocytes. It has been postulated that mixed lymphocyte reactions, which take place between the lymphocytes of the donor and the patient in vivo, are an important stimulus for theimmunization to occur. Leukocyte depletion of blood products (red cells, platelets) is therefore advicedto prevent it. This can be done by differential centrifugation, but also by cotton wool filtration. However the best method is not yet know and controlled studies are badly needed.
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Salman, J., T. Kaufeld, K. Aburahma, C. Bara, A. Niehaus, R. Poyanmehr, M. Franz, et al. "Treatment of ANTI-HLA Donor-Specific Antibodies and Antibody-Mediated Rejection in Heart Transplantation: A Single-Center 3-Year Experience." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725801.
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Brace, L. D., J. Fareed, and D. Hoppensteadt. "EFFECTS OF THROMBOXANE PATHWAY ANTAGONISTS ON HEPARIN-INDUCED PLATELET AGGREGATION (H-IPA) AND TESTING FOR HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643383.
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We have reported that heparin and heparin fractions can induce platelet aggregation (PA) in a substantial number of normal healthy drug-free donors. H-IPA was shown to depend upon the molecular weight and concentration of the heparin preparation used, but its mechanism remains unknown. Therefore, we performed experiments with antagonists of the thromboxane pathway to determine whether arachidonic acid metabolites contribute to H-IPA. When indomethacin or 13-azaprostanoic (a thromboxane receptor anatagonist) was added to the PRP of donors whose platelets had been shown to aggregate in response to heparin, H-IPA was completely inhibited: heparin (bovine or porcine) caused 75% PA, while pretreatment with indomethacin or 13-APA reduced the response to 6%. Similarly, if the same donors ingested 650 mg aspirin 3 hours prior to phlebotomy, the PA response to heparin was reduced to approx. 10%. These results demonstrate that at least part of the mechanism of H-IPA is mediated through thromboxane generation. However, the mechanism by which'heparin stimulates thromboxane production in platelets remains unknown.In some patients, heparin is known to induce an immune response that causes severe thrombocytopenia (HIT) and is associated with arterial and venous thrombosis. Fratantoni, et al. (Blood 45:395-401, 1975) have introduced a PA method for the diagnosis of HIT. We have used a modification of this method to show that the PA observed when heparin is added to a mixture of normal donor PRP and HIT patient’s serum or plasma can be inhibited by antagonists of the thromboxane pathway. When normal donor PRP was pretreated with indomethacin or 13-APA and then mixed with serum from a HIT patient (290 uL PRP:160 uL serum), the PA response to heparin was reduced from 75% to 10% or less. Similarly, if the PRP donors ingested 650 mg aspirin prior to phlebotomy, PA in the HIT test was reduced from 75% to 10% or less. Thus, the interaction of heparin with the antibody and platelets causes thromboxane generation and leads to PA. Cyclo-oxygenase specific antiplatelet drugs and inhibitors of thromboxane generation may be useful in the clinical management of HIT and H-IPA.
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Seidl, S. "SCREENING PROCEDURES TO PREVENT TRANSMISSION OF HEPATITIS B, NON-A,NON-B, AND AIDS BY BLOOD TRANSFUSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644753.
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Although the number of infectious agents capable of being transmitted through blood and blood products is vast, only a few cause problems in recipients of a magnitude which warrants the need for screening tests. The most important agents are Hepatitis B Virus (HBV), Hepatitis non-A,non-B (HNANB) - agents causing posttransfusion hepatitis (PTH) and the human immundeficiency viruses (HIV) responsible for transfusion associated AIDS (TAA).PTH: Prospective studies in open-heart-surgery patients demonstrated a high prevalence (8-17%) *in Spain, Italy, the United States and Israel whereas low percentages (2-5%) were observed in Australia, Finland and West-Germany. Among haemophiliacs acute and chronic hepatitis is a rather frequent complication. Serologic markers of HBV infection have been observed in the majority of patients. Since HBsAg screening has been introduced most cases of PTH (>90%) are due to infection with HNANB-agents. For this type of hepatitis no specific assay exists. It has been suggested that surrogate tests (ALT, anti-HBc screening) might serve as interim screening measure. In prospective studies in the USA a correlation has been observed between donor ALT and recipient hepatitis, but not more than 30% of PTH can be prevented at a loss of 1,5 to 3,0% of the donor population. Similar data have been reported when blood donors were screened for anti-HBc. There was a significantly higher incidence of PTH in recipients receiving at least one unit of anti HBc positive blood. This was recently confirmed in a study in which patients received blood with ALT-levels below 30 IU/ml. The incidence of HNANB was 2,1% after transfusion with anti HBc negative blood whereas 10,1% developed HNANB when anti HB positive blood was transfused (P=< 0.0001). However, these two markers (ALT, anti HBc) do not identify the same NANB carrier population. - ALT screening and testing for anti-HBc have been recently instituted in the USA as “surrogate tests” for detecting HNANB carriers.TAA: Among the total number of AIDS cases there ist a small percentage caused by transfusion of blood and blood products. In the USA approximately 2% of TAA have been reported, 1 % of AIDS patients are haemophiliacs but the majority of haemophiliacs are HIV-antibody positive. According to a survey of the Council of Europe (March 1986) the percentages of HIV positive European haemophiliacs varies between 4 to 8% (Belgium, Norway) and 30 to 60% in other European countries. The number of TAA-cases is around 1%, AIDS among European haemophiliacs has been observed up to 5% of the total AIDS cases. - Screening for HIV antibodies in blood donors was introduced in most European countries and the USA in early summer 1985, but several thousands of recipients of HIV positive blood (issued before) are now virus carriers. This has been confirmed in “look back” programmes: A substantial number of recipient (50 to 90%) has been found to be HIV positive.-A major disadvantage of the HIV antibody test is the fact that antibodies appear several weeks after infection. The gap between infection and detecting HIV antibodies may be reduced by an antigen test, which recognizes the HIV infection as early as two weeks after infection. - The recent detection of HIV 2 implies the necessity of developing tests for the identification of variants of HIV.