Transplantation Immunology (Hillebrands, Sanders, Kroesen)
27 important questions on Transplantation Immunology (Hillebrands, Sanders, Kroesen)
The location of a graft can be orthotopic or heterotopic. What is the difference?
Heterotopic means that graft is not placed in its "original" place. For example a kidney transplantation where the dysfunctional kidney is left in the recipient.
What is the difference between a autograft, isograft/syngeneic graft, allograft, and xenograft?
Isograft -> between genetically identical individuals, for example monozygotic twins
allograft -> between different member of the same species
xenograft -> between two different species, for examples human and pig
Why was the first kidney transplantation in 1954 a succes?
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Name four challenges of solid organ transplantation
- Donor shortage
- Donor organ preservation
- Graft rejection
Is graft rejection mediated by the adaptive or innate immune system? And by which cell is this primarily mediated?
Primarily T cell-mediated.
Based on MHC polymorphic genes, which grafts are rejected?
Graft from F1 hybrid is rejected by parental strain. (So MHCaxb rejects the graft from MHCa and MHCb)
An allo-response is an extremely strong response (responding T-cell: 1-10% vs 0.001-0.0001%) Why do so many T cells respond to allo-MHC?
- no negative selection of T cells with affinity for allo-MHC (in contrast with self-MHC)
- higher density of alloantigens of allogeneic APC
- self peptides presented in allo MHC will also be recognized
- alloresponse is mediated (in part) by expanded clones of (memory) T cells
What happens during direct recognition of allo-MHC by T cells?
T cell (both CD4+ (classII) and CD8+ (classI) recognized unprocessed allogeneic MHC molecule on graft APC.
NO NEED HOST APCs!!
What are the different outcomes of direct and indirect recognition of alloMHC?
Indirect alloantigen recognition leads to:
- antibody-mediated injury to graft cells
- inflammation-mediated injury to graft
What happens during indirect recognition of alloMHC by T cells?
2) Self APC present the allo-MHC bound to self MHC molecule.
3) Alloreactive T cell reacts (CD8+)
What are the basic steps from sensitation to graft rejection?
2) Activation of T cells, generation of effector T cells by direct and indirect presentation
3) Migration of effector T cells to allograft
4) Killing of graft tissue cells and cytokine secretion lead to graft rejection.
What are the characteristic of hyperacute rejection?
- Pre-existing antibodies against endothelial antigens (for example bloodgroup antigens(carbohydrates), MHC and mHC antigens (proteins) and xeno-antigens.
leads to complement activation -> thrombosis, endothelial damage, inflammation -> occlusion
Acute rejection is a cell- and/or antibody-mediated response that occurs days/weeks after transplantation.
Describe the characteristics of acute cellular rejection.
A parenchymal infiltrate of CD4+ T cells (Th1, Th17) and CD8+ CTL causes recruitment of inflammatory cells (macrophages and neutrophils) and lysis.
-Parenchymal cell damage, interstitial inflammation.
Acute rejection is a cell- and/or antibody-mediated response that occurs days/weeks after transplantation.
Describe the characteristics of acute antibody-mediated rejection.
Antibody binding to endothelium --> complement activation --> lysis and thrombus formation
Antibody binding to Fc-R on neutrophils and NK cells --> lysis endothelial cells.
- Endotheliitis
What are the characteristics of chronic graft rejection?
- Multi factorial process (CD4+ T cells, cytokines, macrophages)
- Chronic inflammatory reaction in vessel wall --> fibrosis and transplant vasculopathy (graft arteriosclerosis) caused by the proliferation of vascular smooth muscle cells (VSMC)
How can graft rejection be prevented and treated?
- Preserving donor organ quality
- Suppression of the immune system (immunosuppressive drugs)
The graft survival rates after use of Cyclosporine showed a positive effect. What is the immunosuppressive mechanism behind this?
What are other mechanisms of immunosuppressive medicine on T cells besides cyclosporine?
- killing of proliferating cells (antimetabolites)
- depletion of T cells
- costimulatory blockade (B7)
How can B cell activity be suppressed?
- plasmapheresis
What is the "dark side" of immunosuppression?
- B cell-derived lymphomas
- diabetes, hypertension
- cardiovascular disease
- nephrotoxicity
Who can donate organs?
- non heart beating donors
- living donors
Organ survival is determined by:
- presence of HLA-antibodies in the recipient
- immunosuppressive medication
From what events are HLA-antibodies formed?
- bloodtransfusion
- pregnancy
- previous transplantations
HLA-typing is the combination of all HLA-molecules expressed by an individual. There are alleles in HLA-class I and HLA-class II,
which are they? And what is the maximal possibility of different HLA-molecules?
HLA-class II: DR, DP, DQ: maximal 6 HLA alleles
total: maximal possibilities: 12 different HLA-molecules
What HLA linkage disequilibrium is the strongest between which alleles?
DR- and DQ-locus
What are two forms of analysis of HLA-antibodies?
= incubation of patient-serum with lymphocytes of a selected panel of individuals. least sensitive but clinically most relevant.
- luminex single antigen assay (LSA)
= incubation of patient serum with beads, coated with specific HLA-molecules. highly sensitive and discriminative between specific HLA-molecules.
Which HLA polymorphism is on a higher level, genetic or protein?
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