Transplant Immunology: Basic Immunology and Clinical Practice

2020 ◽  
Author(s):  
David P Foley ◽  
Lung-Yi Lee

Engraftment of a transplanted organ into an allogeneic host triggers a cascade of immunologic responses in the host that are designed to facilitate graft rejection. Modern donor-to-host matching techniques and immunosuppression protocols have successfully tempered this natural immune response so that graft survival has dramatically improved. However, optimizing graft survival by precisely downregulating the host response to graft rejection while preserving host immune defenses against pathologic and infectious agents remains poorly understood and elusive in current clinical practice. This review discusses transplant immunology with respect to host versus graft and the basis of allorecognition, as well as clinical management of the transplanted allograft. Figures show human leukocyte antigen (HLA), direct allorecognition, T cell receptor and CD3, T cell–associated second messenger signaling pathway, CD8 molecules directly ligating class I HLAs and CD4 molecules directly binding HLA class II, detection of alloantibodies by enzyme-linked immunosorbent assay or flow cytometry, recipient-donor crossmatch, histopathology of kidney allograft with antibody-mediated rejection, and an algorithm for assessment and management of renal allograft rejection.  This review contains 9 figures, 6 tables and 61 references. Keywords: Transplantation, immunology, human leukocyte antigen, crossmatch, donor, acute rejection, chronic rejection

2020 ◽  
Author(s):  
Lung-Yi Lee ◽  
David P Foley

Engraftment of a transplanted organ into an allogeneic host triggers a cascade of immunologic responses in the host that are designed to facilitate graft rejection. Modern donor-to-host matching techniques and immunosuppression protocols have successfully tempered this natural immune response so that graft survival has dramatically improved. However, optimizing graft survival by precisely downregulating the host response to graft rejection while preserving host immune defenses against pathologic and infectious agents remains poorly understood and elusive in current clinical practice. This review discusses transplant immunology with respect to host versus graft and the basis of allorecognition, as well as clinical management of the transplanted allograft. Figures show human leukocyte antigen (HLA), direct allorecognition, T cell receptor and CD3, T cell–associated second messenger signaling pathway, CD8 molecules directly ligating class I HLAs and CD4 molecules directly binding HLA class II, detection of alloantibodies by enzyme-linked immunosorbent assay or flow cytometry, recipient-donor crossmatch, histopathology of kidney allograft with antibody-mediated rejection, and an algorithm for assessment and management of renal allograft rejection.  This review contains 9 figures, 6 tables and 61 references. Keywords: Transplantation, immunology, human leukocyte antigen, crossmatch, donor, acute rejection, chronic rejection


2020 ◽  
Author(s):  
David P Foley ◽  
Lung-Yi Lee

Engraftment of a transplanted organ into an allogeneic host triggers a cascade of immunologic responses in the host that are designed to facilitate graft rejection. Modern donor-to-host matching techniques and immunosuppression protocols have successfully tempered this natural immune response so that graft survival has dramatically improved. However, optimizing graft survival by precisely downregulating the host response to graft rejection while preserving host immune defenses against pathologic and infectious agents remains poorly understood and elusive in current clinical practice. This review discusses transplant immunology with respect to host versus graft and the basis of allorecognition, as well as clinical management of the transplanted allograft. Figures show human leukocyte antigen (HLA), direct allorecognition, T cell receptor and CD3, T cell–associated second messenger signaling pathway, CD8 molecules directly ligating class I HLAs and CD4 molecules directly binding HLA class II, detection of alloantibodies by enzyme-linked immunosorbent assay or flow cytometry, recipient-donor crossmatch, histopathology of kidney allograft with antibody-mediated rejection, and an algorithm for assessment and management of renal allograft rejection.  This review contains 9 figures, 6 tables and 61 references. Keywords: Transplantation, immunology, human leukocyte antigen, crossmatch, donor, acute rejection, chronic rejection


2017 ◽  
Vol 292 (51) ◽  
pp. 21149-21158 ◽  
Author(s):  
Lucy C. Sullivan ◽  
Nicholas G. Walpole ◽  
Carine Farenc ◽  
Gabriella Pietra ◽  
Matthew J. W. Sum ◽  
...  

Immunity ◽  
2012 ◽  
Vol 37 (4) ◽  
pp. 611-621 ◽  
Author(s):  
Sophie E. Broughton ◽  
Jan Petersen ◽  
Alex Theodossis ◽  
Stephen W. Scally ◽  
Khai Lee Loh ◽  
...  

2019 ◽  
Vol 72 (1-2) ◽  
pp. 119-129 ◽  
Author(s):  
Kirsten Geneugelijk ◽  
Eric Spierings

AbstractHuman leukocyte antigen (HLA) mismatches between donors and recipients may lead to alloreactivity after solid organ transplantation. Over the last few decades, our knowledge of the complexity of the HLA system has dramatically increased, as numerous new HLA alleles have been identified. As a result, the likelihood of alloreactive responses towards HLA mismatches after solid organ transplantation cannot easily be assessed. Algorithms are promising solutions to estimate the risk for alloreactivity after solid organ transplantation. In this review, we show that the recently developed PIRCHE-II (Predicted Indirectly ReCognizable HLA Epitopes) algorithm can be used to minimize alloreactivity towards HLA mismatches. Together with the use of other algorithms and simulation approaches, the PIRCHE-II algorithm aims for a better estimated alloreactive risk for individual patients and eventually an improved graft survival after solid organ transplantation.


Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 2227-2236 ◽  
Author(s):  
NA Kernan ◽  
C Bordignon ◽  
G Heller ◽  
I Cunningham ◽  
H Castro-Malaspina ◽  
...  

Abstract Risk factors for graft failure were analyzed in 122 recipients of an allogeneic T-cell-depleted human leukocyte antigen (HLA)-identical sibling marrow transplant as treatment for leukemia. In each case pretransplant immunosuppression included 1,375 to 1,500 cGy hyperfractionated total body irradiation and cyclophosphamide (60 mg/kg/d x 2). No patient received immunosuppression prosttransplant for graft-versus-host disease (GVHD) prophylaxis. Nineteen patients in this group experienced graft failure. The major factors associated with graft failure were transplants from male donors and the age of the patient (or donor). Among male recipients of male donor-derived grafts a low dose per kilogram of nucleated cells, progenitor cells (colony forming unit-GM) and T cells was also associated with graft failure. Additional irradiation to 1,500 cGy, high dose corticosteroids posttransplant, and additional peripheral blood donor T cells did not decrease the incidence of graft failure. In addition, type of leukemia, time from diagnosis to transplant, an intact spleen, or the presence of antidonor leukocyte antibodies did not correlate with graft failure. To ensure engraftment of secondary transplants, further immunosuppression was necessary but was poorly tolerated. However, engraftment and survival could be achieved with an immunosuppressive regimen in which antithymocyte globulin and high dose methylprednisolone were administered both before and after infusions of secondary partially T- cell-depleted marrow grafts.


2019 ◽  
Vol 20 (20) ◽  
pp. 5044 ◽  
Author(s):  
S. M. Shamsul Islam ◽  
Hyoun-Ah Kim ◽  
Bunsoon Choi ◽  
Ju-Yang Jung ◽  
Sung-Min Lee ◽  
...  

It has been reported Human Leukocyte Antigen (HLA) gene polymorphism is a risk factor for the development of Behçet’s disease (BD). In this study, the association of HLA class II subtypes HLA-DP, DQ, DR, and T cell subsets in BD patients with arthritis was evaluated. Frequencies of HLA-DP, DQ, DR positive cells, and T cell subsets in peripheral blood leukocytes (PBL) were measured by flow cytometric analysis in BD, and compared to rheumatoid arthritis as disease controls and healthy controls. Frequencies of HLA-DQ were significantly decreased in whole PBL and granulocytes of BD active patients as compared to healthy controls. In monocytes populations, proportions of HLA-DR positive cells were significantly increased in BD active patients as compared to healthy controls. Proportions of CD4+CCR7+ and CD8+CCR7+ cells were significantly higher in BD active patients than in BD inactive in whole PBL. Frequencies of CD4+CD62L- and CD8+CD62L- cells in lymphocytes were significantly decreased in active BD than those in inactive BD. There were also correlations between disease activity markers and T cell subsets. Our results revealed HLA-DP, DQ, and DR expressing cell frequencies and several T cell subsets were significantly correlated with BD arthritis symptoms.


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