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[PMID]:28832450
[Au] Autor:Kransdorf EP; Pando MJ; Gragert L; Kaplan B
[Ad] Endereço:1 Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA. 2 Division of Laboratory Medicine and Pathology, Mayo Clinic Arizona, Phoenix, AZ. 3 Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA. 4 Division of Nephrology and Hypertension, Mayo Clinic Arizona, Phoenix, AZ.
[Ti] Título:HLA Population Genetics in Solid Organ Transplantation.
[So] Source:Transplantation;101(9):1971-1976, 2017 Sep.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HLAs are fundamental to the adaptive immune response and play critical roles in the cellular and humoral response in solid organ transplantation. The genes encoding HLA proteins are the most polymorphic within the human genome, with thousands of different allelic variants known within the population. Application of the principles of population genetics to the HLA genes has resulted in the development of a numeric metric, the calculated panel-reactive antibody (CPRA) that predicts the likelihood of a positive crossmatch as a function of a transplant candidate's unacceptable HLA antigens. The CPRA is an indispensible measure of access to transplantation for sensitized candidates and is used as the official measure of sensitization for allocation of points in the US Kidney Allocation System and Eurotransplant. Here, we review HLA population genetics and detail the mathematical basis of the CPRA. An understanding of these principles by transplant clinicians will lay the foundation for continued innovation in the care of sensitized patients.
[Mh] Termos MeSH primário: Genética Populacional
Rejeição de Enxerto/genética
Antígenos HLA/genética
Histocompatibilidade
Transplante de Órgãos/métodos
Polimorfismo Genético
[Mh] Termos MeSH secundário: Rejeição de Enxerto/imunologia
Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto
Antígenos HLA/imunologia
Seres Humanos
Isoanticorpos/imunologia
Modelos Genéticos
Transplante de Órgãos/efeitos adversos
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA Antigens); 0 (Isoantibodies)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001830


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[PMID]:28782523
[Au] Autor:Ravindranath MH; Jucaud V; Ferrone S
[Ad] Endereço:Terasaki Foundation Laboratory, Los Angeles, CA, United States. Electronic address: ravimh@terasakilab.org.
[Ti] Título:Monitoring native HLA-I trimer specific antibodies in Luminex multiplex single antigen bead assay: Evaluation of beadsets from different manufacturers.
[So] Source:J Immunol Methods;450:73-80, 2017 Nov.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Luminex single antigen bead (SAB) assay utilizes beadsets coated with a set of cloned and purified HLA molecules, for monitoring serum anti-HLA antibodies. Particularly, the level of serum IgG against native HLA-I trimers (heavy chain (HC) and ß2-microglobulin (ß2m) with a peptide), expressed in allograft tissues is correlated with graft failure. In addition to native trimeric HLAI, the beadsets may carry HC only or the dimeric variants, peptide-free HC with ß2m and ß2m-free HC with or without peptides. Currently, three different HLA-I coated beadsets have been produced commercially. The HLA antigen density on one beadset was reported to be approximately 50% of that present on another beadset as evidenced by the binding of an anti-HLA-I mAb W6/32. To date, no efforts have been made to compare the relative distribution of HLA-I variants in these three beadsets. In this study, using monoclonal antibodies (W6/32, HC-10 and TFL-006) that can distinguish the structural variants based on their epitope specificities, the nature of the variants in the three beadsets were comparatively evaluated. One beadset (Beadset A, see Materials and methods for Brand and Manufacturer's names) (W6/32+/HC-10+/TFL-006+) carried at least three variants, while beadset B (W6/32+/HC-10+/TFL-006-) carried two (peptide-associated and peptide-free ß2m-HC) and the beadset C (W6/32+/HC-10-/TFL-006-) carried exclusively the HLA-I trimer suggesting its usefulness for specific monitoring native HLA-I trimer antibodies. Because of the salient differences in the variants coated on the different beadsets, it would be warranted to investigate, if these differences are clinically relevant for monitoring serum anti-HLA antibodies in sensitized patients waiting for donor organs and in allograft recipients (274).
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Especificidade de Anticorpos
Epitopos
Antígenos HLA/imunologia
Teste de Histocompatibilidade/instrumentação
Histocompatibilidade
Imunoensaio/instrumentação
Imunoglobulina G/imunologia
Isoanticorpos/imunologia
[Mh] Termos MeSH secundário: Teste de Histocompatibilidade/normas
Seres Humanos
Imunoensaio/normas
Imunoglobulina G/sangue
Isoanticorpos/sangue
Valor Preditivo dos Testes
Controle de Qualidade
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Epitopes); 0 (HLA Antigens); 0 (Immunoglobulin G); 0 (Isoantibodies)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28686681
[Au] Autor:Littera R; Piredda G; Argiolas D; Lai S; Congeddu E; Ragatzu P; Melis M; Carta E; Michittu MB; Valentini D; Cappai L; Porcella R; Alba F; Serra M; Loi V; Maddi R; Orrù S; La Nasa G; Caocci G; Cusano R; Arras M; Frongia M; Pani A; Carcassi C
[Ad] Endereço:Regional Transplant Center, R. Binaghi Hospital, ASSL Cagliari, ATS Sardegna, Italy.
[Ti] Título:KIR and their HLA Class I ligands: Two more pieces towards completing the puzzle of chronic rejection and graft loss in kidney transplantation.
[So] Source:PLoS One;12(7):e0180831, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Kidney transplantation is a life-saving treatment for patients with end-stage renal disease. However, despite progress in surgical techniques and patient management, immunological rejection continues to have a negative impact on graft function and overall survival. Incompatibility between donors and recipients for human leukocyte antigens (HLA) of the major histocompatibility complex (MHC) generates a series of complex cellular and humoral immune response mechanisms that are largely responsible for rejection and loss of graft function. Within this context, a growing amount of evidence shows that alloreactive natural killer (NK) cells play a critical role in the immune response mechanisms elicited by the allograft. Killer immunoglobulin-like receptors (KIRs) are prominent mediators of NK cell alloreactivity. METHODS AND FINDINGS: A cohort of 174 first cadaveric kidney allograft recipients and their donors were selected from a total cohort of 657 transplanted patients for retrospective immunogenetic analyses. Patients with HLA Class II mismatches were excluded. HLA Class I allele frequencies were compared among patients with chronic rejection, patients with stable graft function and a group of 2388 healthy controls. Activating and inhibitory KIR gene frequencies, KIR haplotypes, KIR-HLA ligand matches/mismatches and combinations of recipient KIRs and donor HLA Class I ligands were compared among patients with and without chronic rejection and a group of 221 healthy controls. Patients transplanted from donors homozygous for HLA-C1 antigens had a significantly higher risk for chronic rejection than patients transplanted from donors homozygous or heterozygous for HLA-C2 antigens or with epitopes belonging to the HLA-Bw4 ligand group. The Kaplan-Meier curves obtained by dividing the patients into 3 groups according to the presence or absence of one or both of the combinations of recipient KIRs and donor HLA ligands (rKIR2DL1/dHLA-C2 and rKIR3DL1/dHLA-Bw4) showed a significantly higher cumulative incidence of chronic rejection in the group of patients completely lacking these functional units. These patients showed a progressively stronger decline in modification of diet in renal disease-estimated glomerular filtration rate. CONCLUSIONS: KIR genotyping should be performed at the time of enrolment of patients on the waiting list for organ transplantation. In our study, a significantly higher risk of chronic rejection after kidney transplantation was observed when recipient (r) and donor (d) pairs completely lacked the two functional rKIR-dHLA ligand combinations rKIR2DL1/dHLA-C2 and rKIR3DL1/dHLA-Bw4. This immunogenetic profile corresponds to low levels of NK cell inhibition. Therefore, patients with this high risk profile could benefit from immunosuppressive therapy aimed at reducing NK-cell cytotoxicity.
[Mh] Termos MeSH primário: Rejeição de Enxerto/genética
Antígenos HLA-B/imunologia
Antígenos HLA-C/imunologia
Transplante de Rim
Receptores KIR2DL1/imunologia
Receptores KIR3DL1/imunologia
[Mh] Termos MeSH secundário: Adulto
Cadáver
Estudos de Casos e Controles
Feminino
Expressão Gênica
Taxa de Filtração Glomerular
Rejeição de Enxerto/imunologia
Rejeição de Enxerto/patologia
Sobrevivência de Enxerto/genética
Antígenos HLA-B/genética
Antígenos HLA-C/genética
Histocompatibilidade
Seres Humanos
Falência Renal Crônica/imunologia
Falência Renal Crônica/patologia
Falência Renal Crônica/cirurgia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/patologia
Ligantes
Masculino
Meia-Idade
Receptores KIR2DL1/genética
Receptores KIR3DL1/genética
Transplante Homólogo
Doadores não Relacionados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-B Antigens); 0 (HLA-Bw4 antigen); 0 (HLA-C Antigens); 0 (KIR2DL1 protein, human); 0 (KIR3DL1 protein, human); 0 (Ligands); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR3DL1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180831


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[PMID]:28604446
[Au] Autor:Young JS; McIntosh C; Alegre ML; Chong AS
[Ad] Endereço:1 Section of Transplantation, Department of Surgery, The University of Chicago, Chicago, IL. 2 Section of Rheumatology, Department of Medicine, The University of Chicago, Chicago, IL.
[Ti] Título:Evolving Approaches in the Identification of Allograft-Reactive T and B Cells in Mice and Humans.
[So] Source:Transplantation;101(11):2671-2681, 2017 Nov.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Whether a transplanted allograft is stably accepted, rejected, or achieves immunological tolerance is dependent on the frequency and function of alloreactive lymphocytes, making the identification and analysis of alloreactive T and B cells in transplant recipients critical for understanding mechanisms, and the prediction of allograft outcome. In animal models, tracking the fate of graft-reactive T and B cells allows investigators to uncover their biology and develop new therapeutic strategies to protect the graft. In the clinic, identification and quantification of graft-reactive T and B cells allows for the early diagnosis of immune reactivity and therapeutic intervention to prevent graft loss. In addition to rejection, probing of T and B cell fate in vivo provides insights into the underlying mechanisms of alloimmunity or tolerance that may lead to biomarkers predicting graft fate. In this review, we discuss existing and developing approaches to track and analyze alloreactive T and B cells in mice and humans and provide examples of discoveries made utilizing these techniques. These approaches include mixed lymphocyte reactions, trans-vivo delayed-type hypersensitivity, enzyme-linked immunospot assays, the use of antigen receptor transgenic lymphocytes, and utilization of peptide-major histocompatibility multimers, along with imaging techniques for static multiparameter analysis or dynamic in vivo tracking. Such approaches have already refined our understanding of the alloimmune response and are pointing to new ways to improve allograft outcomes in the clinic.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto
Técnicas Imunológicas
Ativação Linfocitária
Transplante de Órgãos
Linfócitos T/imunologia
Tolerância ao Transplante
[Mh] Termos MeSH secundário: Aloenxertos
Animais
Linfócitos B/efeitos dos fármacos
Linfócitos B/metabolismo
Rejeição de Enxerto/sangue
Rejeição de Enxerto/imunologia
Sobrevivência de Enxerto/efeitos dos fármacos
Histocompatibilidade
Seres Humanos
Imunossupressores/uso terapêutico
Isoanticorpos/sangue
Ativação Linfocitária/efeitos dos fármacos
Camundongos
Modelos Animais
Transplante de Órgãos/efeitos adversos
Plasmócitos/imunologia
Fatores de Risco
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
Tolerância ao Transplante/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (Isoantibodies)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001847


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[PMID]:28574903
[Au] Autor:Chhabra AY; Leventhal J; Merchak AR; Ildstad S
[Ad] Endereço:1 Institute for Cellular Therapeutics, University of Louisville, Louisville, KY. 2 Comprehensive Transplant Center, Northwestern Memorial Hospital, Chicago, IL.
[Ti] Título:HSCT-Based Approaches for Tolerance Induction in Renal Transplant.
[So] Source:Transplantation;101(11):2682-2690, 2017 Nov.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal transplantation has become the preferred treatment for end stage kidney failure. Although short-term graft survival has significantly improved as advances in immunosuppression have occurred, long-term patient and graft survival have not. Approximately only 50% of renal transplant recipients are alive at 10 years due to the toxicities of immunosuppression and alloimmunity. Emerging research on cell-based therapies is opening a new door for patients to receive the organs they need without sacrificing quality of life and longevity because of drug-based immunosuppression. Research has focused on inducing tolerance, a state in which the body accepts the transplant and graft function is stable. Cell-based therapies to facilitate chimerism and achieve tolerance in major histocompatibility disparate recipients have been developed in mouse, swine, canine, and nonhuman primate models. These findings are now being translated into the clinic in several trials currently underway. Protocols that use a combination of traditional therapeutic agents paired with cell populations including hematopoietic stem cells, regulatory T cells, and facilitating cells are being conducted with the objective to harness the donor immune system to protect the transplanted tissue. The benefits and feasibility of the clinical application of cell-based therapy has been demonstrated, and promising results have been achieved. Here we discuss the preclinical work that has led to the clinical application of the various approaches and a summary of the most current clinical data from groups throughout the world.
[Mh] Termos MeSH primário: Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto
Transplante de Células-Tronco Hematopoéticas
Transplante de Rim
Tolerância ao Transplante
[Mh] Termos MeSH secundário: Animais
Rejeição de Enxerto/imunologia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Histocompatibilidade
Seres Humanos
Isoanticorpos/imunologia
Transplante de Rim/efeitos adversos
Modelos Animais
Especificidade da Espécie
Fatores de Tempo
Pesquisa Médica Translacional
Quimeras de Transplante/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Isoantibodies)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001837


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[PMID]:28557957
[Au] Autor:Zhang H; Huang E; Kahwaji J; Nast CC; Li P; Mirocha J; Thomas DL; Ge S; Vo AA; Jordan SC; Toyoda M
[Ad] Endereço:1 Transplant Immunology Laboratory, Cedars-Sinai Medical Center, Los Angeles, CA. 2 Comprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, CA. 3 Department of Nephrology, Kaiser-Permanente Los Angeles Medical Center, Los Angeles, CA. 4 Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA. 5 Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA. 6 Biostatistics and Bioinformatics Research Center, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
[Ti] Título:Plasma Exosomes From HLA-Sensitized Kidney Transplant Recipients Contain mRNA Transcripts Which Predict Development of Antibody-Mediated Rejection.
[So] Source:Transplantation;101(10):2419-2428, 2017 Oct.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sensitization to HLA remains a significant immunologic barrier to successful transplantation. Identifying immune mechanisms responsible for antibody-mediated rejection (AMR) is an important goal. Here, we explored the possibility of predicting the risk for AMR by measuring mRNA transcripts of AMR-associated genes in plasma exosomes from kidney transplant patients. METHODS: Total RNA was extracted from exosomes purified from 152 ethylenediaminetetraacetic acid-plasma samples of 64 patients (18 AMR, 8 cell-mediated rejection [CMR], 38 no rejection in desensitized [DES] and non-DES control groups) for reverse transcription into cDNA, preamplification and then real time quantitative polymerase chain reaction (qPCR) for 21 candidate genes. The mRNA transcript levels of each gene were calculated. Comparisons were made among 4 patient groups for each gene and also for a gene combination score based on selected genes. RESULTS: Among 21 candidate genes, we identified multiple genes (gp130, CCL4, TNFα, SH2D1B, CAV1, atypical chemokine receptor 1 [duffy blood group]) whose mRNA transcript levels in plasma exosomes significantly increased among AMR compared with CMR and/or control patients. A gene combination score calculated from 4 genes of gp130, SH2D1B, TNFα, and CCL4 was significantly higher in the AMR than the CMR (P < 0.0001) and no rejection control groups (P < 0.01 vs DES control, P < 0.05 vs non-DES control). CONCLUSIONS: Our results suggest that plasma exosomes may contain information indicating clinical conditions of kidney transplant patients. mRNA transcript profiles based on gp130, SH2D1B, TNFα, and CCL4 in plasma exosomes may be used to predict on-going and/or imminent AMR.
[Mh] Termos MeSH primário: Exossomos/metabolismo
Rejeição de Enxerto/sangue
Antígenos HLA/imunologia
Histocompatibilidade
Isoanticorpos/sangue
Transplante de Rim/efeitos adversos
RNA Mensageiro/sangue
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Quimiocina CCL4/genética
Receptor gp130 de Citocina/genética
Exossomos/genética
Feminino
Perfilação da Expressão Gênica/métodos
Marcadores Genéticos
Rejeição de Enxerto/genética
Rejeição de Enxerto/imunologia
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Medição de Risco
Fatores de Risco
Fatores de Transcrição/genética
Resultado do Tratamento
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL4 protein, human); 0 (Chemokine CCL4); 0 (Genetic Markers); 0 (HLA Antigens); 0 (IL6ST protein, human); 0 (Isoantibodies); 0 (RNA, Messenger); 0 (SH2D1B protein, human); 0 (Transcription Factors); 0 (Tumor Necrosis Factor-alpha); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001834


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[PMID]:28474441
[Au] Autor:Dufour C
[Ad] Endereço:Haematology Unit, G. Gaslini Children's Research Hospital, Genova, Italy.
[Ti] Título:How I manage patients with Fanconi anaemia.
[So] Source:Br J Haematol;178(1):32-47, 2017 Jul.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fanconi Anaemia is a rare, genetic heterogeneous multisystem disease that is the most common congenital syndrome of marrow failure. Twenty genes have been reported to cause the disease. Remarkable progress has been made over the last 20 years in the understanding of the genetic and pathophysiological mechanisms. Unfortunately, these advances have not been completely paralleled by advances in medical treatment, where the most important component remains stem cell transplantation. This therapy, although contributing to long-term negative effects, such as increased occurrence of late malignancies, is the only current option capable of prolonging the survival of patients. In spite of relevant recent progress in matched unrelated donor transplants, the largest studies with longer follow-up still show a superiority of matched sibling donor transplants with a success rate, in selected cohorts, of over 90%. This article reviews different aspects of the disease, including genetics, diagnosis and treatment options, with special focus on stem cell transplantation, comprehensive post-diagnosis management, decision-making processes and long-term follow-up.
[Mh] Termos MeSH primário: Anemia de Fanconi/terapia
[Mh] Termos MeSH secundário: Anormalidades Múltiplas/diagnóstico
Anormalidades Múltiplas/genética
Tomada de Decisão Clínica/métodos
Anemia de Fanconi/diagnóstico
Anemia de Fanconi/genética
Proteínas de Grupos de Complementação da Anemia de Fanconi/genética
Histocompatibilidade
Teste de Histocompatibilidade
Seres Humanos
Mutação
Transplante de Células-Tronco/efeitos adversos
Transplante de Células-Tronco/métodos
Doadores de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fanconi Anemia Complementation Group Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14615


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[PMID]:28471872
[Au] Autor:Opelz G; Döhler B; Middleton D; Süsal C; A Collaborative Transplant Study Report
[Ad] Endereço:1 Institute of Immunology, University of Heidelberg, Heidelberg, Germany. 2 Royal Liverpool Hospital & University of Liverpool, Liverpool, United Kingdom.
[Ti] Título:HLA Matching in Pediatric Kidney Transplantation: HLA Poorly Matched Living Donor Transplants Versus HLA Well-Matched Deceased Donor Transplants.
[So] Source:Transplantation;101(11):2789-2792, 2017 Nov.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Based on an analysis of 542 pediatric kidney transplants recorded by the UK Transplant Registry from 2000 to 2012, it was concluded that the survival rate of HLA poorly matched living donor transplants is not inferior to that of HLA well-matched deceased donor transplants. METHODS: We analyzed the impact of HLA matching on kidney graft survival in 3627 pediatric living donor transplants performed during 2000 to 2015 using the data of the Collaborative Transplant Study. The impact of HLA mismatches on graft survival was analyzed and survival rates of transplants from poorly matched living donors were compared with those from well-matched deceased donors. Multivariate Cox regression analysis was used to account for the influence of confounders. RESULTS: HLA matching had a statistically significant impact on graft survival of pediatric kidney transplants (P < 0.001). Ten-year graft survival of pediatric transplants from living donors with 4 to 6 HLA-A+B+DR mismatches was significantly worse than that of transplants from well-matched deceased donors with 0 to 1 HLA mismatch (log rank, P = 0.006). CONCLUSIONS: In pediatric kidney transplantation, graft survival of kidneys from deceased donors with 0 to 1 HLA mismatches compares favorably with that of grafts from living donors with 4 to 6 HLA mismatches. If possible, living donor pediatric kidney transplants should be performed from donors with fewer than 4 HLA-A+B+DR mismatches.
[Mh] Termos MeSH primário: Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto
Antígenos HLA/imunologia
Histocompatibilidade
Transplante de Rim/métodos
Doadores Vivos
[Mh] Termos MeSH secundário: Adolescente
Fatores Etários
Criança
Pré-Escolar
Feminino
Rejeição de Enxerto/imunologia
Teste de Histocompatibilidade
Seres Humanos
Lactente
Recém-Nascido
Estimativa de Kaplan-Meier
Transplante de Rim/efeitos adversos
Masculino
Análise Multivariada
Modelos de Riscos Proporcionais
Medição de Risco
Fatores de Risco
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA Antigens)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001811


  9 / 6781 MEDLINE  
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[PMID]:28444735
[Au] Autor:Bogunia-Kubik K; Lacina P
[Ad] Endereço:Laboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
[Ti] Título:From genetic single candidate gene studies to complex genomics of GvHD.
[So] Source:Br J Haematol;178(5):661-675, 2017 Sep.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Graft-versus-host disease (GvHD) is a serious complication affecting the recipients of allogeneic haematopoietic stem cells. In this present review we attempt to summarize the current knowledge on the effect of the donor and recipient genotypes on GvHD, starting from human leucocyte antigen (HLA) matching for an optimal donor selection, typing of non-classical HLA and minor histocompatibility antigens through the polymorphic variations in genes coding for non-HLA proteins contributing to the development of GvHD and response to treatment. The results of recent Candidate Gene Studies (CGS) and Genome-Wide Association Studies (GWAS) are presented and discussed.
[Mh] Termos MeSH primário: Doença Enxerto-Hospedeiro/genética
[Mh] Termos MeSH secundário: Citocinas/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Genômica/métodos
Antígenos HLA/genética
Histocompatibilidade
Teste de Histocompatibilidade/métodos
Seres Humanos
Antígenos de Histocompatibilidade Menor/genética
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (HLA Antigens); 0 (Minor Histocompatibility Antigens)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14704


  10 / 6781 MEDLINE  
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[PMID]:28424235
[Au] Autor:Olofson AM; Chandler RM; Marx-Wood CR; Babcock CA; Dunbar NM
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
[Ti] Título:Increased alloimmunisation and transfusion reaction reporting in patients with solid-phase panreactivity.
[So] Source:J Clin Pathol;70(11):981-983, 2017 Nov.
[Is] ISSN:1472-4146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Automated solid-phase antibody screening uses red blood cell (RBC) membranes immobilised on polystyrene test wells to detect RBC specific antibodies. Despite its time-saving and labour-saving benefits, this method produces a higher rate of nonspecific reactivity compared with manual screening. Solid-phase panreactivity (SPP) is characterised by panreactivity (ie, all test cells reacting) in solid-phase testing accompanied by a negative autocontrol and a lack of reactivity when the same screening cells are tested in tube. The mechanisms underlying SPP and its clinical significance remain unclear. The goals of this study were to describe the prevalence of SPP at our institution and determine the alloimmunisation and transfusion reaction rates within this population. METHODS: Data were collected on all patients undergoing type and screen testing over a 6-year period. Study patients undergoing subsequent transfusion were evaluated for reported transfusion reactions and development of new alloantibodies. RESULTS: Of the 76 051 patients studied, 0.7% demonstrated SPP of which 11% developed new alloantibodies. The transfusion reaction reporting rate among patients with SPP was 2%. CONCLUSIONS: Our data suggest that patients with SPP have higher rates of reported transfusion reactions and alloantibody development compared with those without SPP.
[Mh] Termos MeSH primário: Tipagem e Reações Cruzadas Sanguíneas/métodos
Transfusão de Eritrócitos/efeitos adversos
Eritrócitos/imunologia
Histocompatibilidade
Isoanticorpos/sangue
Isoantígenos/sangue
Reação Transfusional/etiologia
[Mh] Termos MeSH secundário: Automação Laboratorial
Seres Humanos
Valor Preditivo dos Testes
Reprodutibilidade dos Testes
Estudos Retrospectivos
Fatores de Risco
Reação Transfusional/sangue
Reação Transfusional/imunologia
Carga de Trabalho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isoantibodies); 0 (Isoantigens)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1136/jclinpath-2017-204355



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