Transplantation immunology

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History
Introduction
Classification of grafts
The Immunology of Allogeneic Transplantation
Genetics of graft rejection
Types of rejection
Recognition of Alloantigens
Effector Mechanisms of Allograft Rejection
Prevention of graft rejection
Graft versus host reaction



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Transplantation immunology

  1. 1. Rinkesh Joshi M.Sc Sem : 3 Bioscience ( Micro) 09924113838 Surat, Gujarat.
  2. 2. History Introduction Classification of grafts The Immunology of Allogeneic Transplantation Genetics of graft rejection Types of rejection Recognition of Alloantigens Effector Mechanisms of Allograft Rejection Prevention of graft rejection Graft versus host reaction
  3. 3.  1944 : Medawar showed that skin allograft rejection is a host versus graft response.  1954 : The first successful identical twin transplant of a human kidney was performed by Joseph E. Murray in Boston  1967 : The first successful liver transplant was done by Dr. Thomas E. Starzl  1967 : The first heart transplantation by Christian Barnard  1968 : The first successful bone marrow transplant was done by E. Donnall Thomas
  4. 4. Transplantation is a act of transferring cells, tissue, or organ from one site to another Graft : Implanted cell, tissue or organ Donor : Individual who provides the graft Recipient or host : Individual who receives the graft
  5. 5.  Self tissue is transferred from one body site to another  Antigen present in autograft is same as that present in body  So immune system recognizes the autograft antigen as a self antigen  No immune response is elicited  Autograft survive through out the life  Eg., - Transferring healthy skin to burned area, - Use of healthy blood vessels to replace blocked coronary arteries, - Plastic surgery of skin.
  6. 6. It is also called syngraft Tissue is transferred between genetically identical individuals of same species In isograft the histo compatibility antigens are identical hence the graft survives and not rejected. Eg in human isograft can be performed between two twins.
  7. 7. Tissue is transferred between two genetically different members of same species In allograft histocompatibility antigens are dissimilar hence immune response is elicited and graft is rejected Eg., In humans graft is transferred from one individual to another
  8. 8. Tissue is transferred between two different species Eg., Graft of human transferred to animal In xenografts histocompatibility complex antigens are so different that the graft is more vigorously rejected
  9. 9. • Alloantigens elicit both cell-mediated and humoral immune responses. • Recognition of transplanted cells that are self or foreign is determined by polymorphic genes that are inherited from both parents and are expressed co-dominantly.
  10. 10. Rate of allograft rejection varies according to tissue involved Skin graft are rejected faster than other tissue organ kidney or heart If inbred mouse of strain A is grafted with skin from strain B , Primary graft rejection occur called first set rejection When again strain A is grafted with skin from strain B , Secondary graft rejection occur called second set rejection
  11. 11. Direct recognition of Alloantigens host T cells recognize intact allo-MHC molecules on the surface of the donor cell. host T cells see allo-MHC molecule + allo-peptide as being equivalent in shape to self-MHC + foreign peptide and hence recognize the donor tissue as foreign. This pathway is the dominant pathway.
  12. 12.  Indirect recognition of Alloantigens Donor MHC is processed and presented by recipient APC Basically, donor MHC molecule is handled like any other foreign antigen
  13. 13. Donor APCs migrate to regional lymph nodes and are recognized by the recipient’s T cells Alloreactive T cells in the recipient may be activated and they migrate into the graft and cause graft rejection
  14. 14. Used by immune system to reject allograft It is based on histopathological features or time duration of rejection after transplantation There are three type of patterns 1. Hyperacute Rejection 2. Acute Rejection 3. Chronic Rejection
  15. 15.  Graft is rejected within minutes to hours because vascularization is rapidly destroyed.  It occurs because the recipient has pre-existing antibodies in circulation against the graft.  Which could be induced by prior blood transfusions, multiple pregnancies, prior transplantation, or xenografts.  Antibodies bind with donor endothelial cell.  The antigen-antibody complexes activate the complement system, causing massive thrombosis in the capillaries, which prevents the vascularization of the graft.  The kidney is most susceptible to hyperacute rejection.
  16. 16. 1) 2) 3) 4) 5) Preformed Ab, complement activation, Neutrophil margination, Inflammation, Thrombosis formation.
  17. 17.  Vascular and parenchymal injury mediated by T cells and antibodies that usually begin after the first week of transplantation if there is no immunosuppressant therapy  Antibodies from after transplantation may also contribute to vascular injury.
  18. 18. Occurs in most solid organ transplants o Heart o Kidney o Lung o Liver Characterized by fibrosis and vascular abnormalities with loss of graft function over a prolonged period
  19. 19. Arthrosclerosis Cell proliferation Occlusion
  20. 20. I. II. III. IV. Blood grouping Cytotoxic antibody testing Tissue matching Immunosuppressive drugs (azathioprine,cyclosporine,rapamycin, cortic osteroids)
  21. 21. In some instance the graft tissue elicits an immune response against host antigen and that immune response is called graft versus host reaction Graft versus host reaction brings damage to host cells and host When grafted tissue has mature T cells, they will attack host tissue leading to GVHR.
  22. 22. Graft lymphocytes aggregate in the host lymphoid organs Graft lymphocytes are stimulated by the host lymphocyte Stimulated lymphocytes of graft produce lymphokines Lymphokines activate host T- cell which produce polyclonal b-cell activation Activated b-cell react with the self antigens and cause damage to the host cell
  23. 23. Skin rash Emaciation ( becoming thin) Retarded growth Diarrhoea Hepatomegaly Splenomegaly Increase in bilirubin production Bileducts are damaged anaemia

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