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π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž > Transplantation and Immunosuppressive Drugs > Flashcards

Transplantation and Immunosuppressive Drugs Flashcards

1
Q

What is the definition of transplantation?

A

➝ The introduction of biological material (organs, tissues, cells) into an organism

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2
Q

What is an autologous transplant?

A

➝ transplantation of tissue from one part of the organism to another part of the same organism

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3
Q

What is an example of an autologous transplant?

A

➝ Skin graft

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4
Q

What is a syngeneic transplant?

A

➝ donor material transplanted into the recipient when the donor and recipient are genetically identical

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5
Q

What is an allogenic transplant?

A

➝ Donors and recipients are from the same species but genetically different

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6
Q

What is a xenogenic transplant?

A

➝ donor and recipient are different species

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7
Q

What are immune responses to transplant caused by?

A

➝ genetic differences between the donor and recipient

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8
Q

What are human MHC proteins called?

A

➝ human leukocyte antigen

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9
Q

On what chromosome is HLA found?

A

➝ chromosome 6

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10
Q

How many MHC Class I alleles are there?

A

➝ 3

➝ A, B, C

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11
Q

How many MHC Class II alleles are there and what structures do they form?

A

➝ 3

➝ heterodimers of two proteins

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12
Q

Which cells in the body express both MHC class I and II?

A

➝ White blood cells

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13
Q

What are the MHC Class II alleles?

A 
➝ DRA
➝ DRB
➝ DPA
➝ DPB
➝ DQA
➝ DQB
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14
Q

What is needed to define epitopes on HLA?

A

➝ next generation sequencing

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15
Q

What do T cells recognise?

A

➝ short peptide fragments that are presented to them by MHC proteins

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16
Q

What can professional APCs do with external proteins?

A

➝ internalise them and cross present them on the MHC class I pathway

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17
Q

What does MHC class II bind?

A

➝ Fragments of proteins which have been taken up by endocytosis

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18
Q

What does MHC Class I bind?

A

➝ Fragments of intracellular proteins

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19
Q

What is the function of CLIP?

A

➝ Maintains the shape of the HLA until the peptides are ready to bind

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20
Q

Describe indirect allo-recognition?

A

➝ The recipient cell has self HLA on its cell if the cell expresses the self peptide as normal cells do there is no immune response
➝ the TCR will be quiescent
➝ When self HLA presents a peptide (eg influenza peptide) an immune response will occur against the influenza
➝ if the recipient has a transplantation and the self HLA can present a peptide from the donor HLA molecule there is indirect allo-recognition

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21
Q

What is indirect allo-recognition?

A

➝ TCR of recipient detecting non-self peptide on self HLA

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22
Q

Describe direct allo-recognition?

A

➝ A recipient has transplanted tissue which contain donor immune cells
➝ If they have been perfectly matched the donor HLA is the same as the recipient HLA and there is no reaction
➝ when there is an unmatched donor there is direct allo-recognition
➝ the TCR from the recipients T cells will detect the MHC
➝ even if the peptide isn’t recognised as foreign (because it is from a conserved region) the unmatched HLA activates the T cells

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23
Q

What is direct allo-recognition?

A

➝ TCR of the recipient reacting to donor HLA molecules

24
Q

How many MHC loci are usually matched?

A

➝ 4/6 MHC class II loci

25
Q

Why are live donors better than dead donors?

A

➝ Recipients will have a history of disease which results in a degree of inflammation
➝ organs from deceased donors are likely to be inflamed due to ischemia

26
Q

What are the three types of graft rejection?

A

➝ Hyperacute rejection
➝ Acute rejection
➝ Chronic rejection

27
Q

When does hyperacute rejection occur?

A

➝ within a few hours of transplant

28
Q

What organs does hyperacute rejection usually occur with?

A

➝ highly vascularised organs

29
Q

How does hyperacute rejection occur and what is needed?

A

➝ requires pre-existing antibodies usually to ABO blood group antigens or MHC I proteins
➝ ABO antigens are expressed on endothelial cells of blood vessels

30
Q

What are the three ways antibodies to MHC can arise?

A

➝ Pregnancy
➝blood transfusion
➝ previous transplant

31
Q

What does recognition of the Fc region lead to?

A

➝ Complement activation
➝ antibody dependent cellular cytotoxicity (Fc receptors on NK cells)
➝ Phagocytosis (Fc receptors on macrophages)

32
Q

How do thrombi develop in hyperacute rejction?

A

➝ Antibodies bind to endothelial cells
➝ Complement fixation
➝ Accumulation of innate immune cells
➝ Endothelial damage, platelets accumulate, thrombi develop

33
Q

What causes acute rejection?

A

➝ T cell response develops as a result of MHC mismatch

34
Q

Describe how transplants are destroyed by acute rejection?

A

➝ Dendritic cells migrate to secondary lymphoid tissue where they encounter circulating effector T cells
➝ Macrophages and CTL increase inflammation and destroy the transplant

35
Q

When does chronic rejection occur?

A

➝ months or years after the transplant

36
Q

What does chronic rejection result from?

A

➝ Indirect allorecognition of foreign MHC/HLA

37
Q

Describe how chronic rejection occurs?

A

➝ Blood vessel walls thickened, lumina narrowed and loss of blood supply
➝ correlates with the presence of antibodies to MHC-I
➝ Donor derived cells die
➝ membrane fragments containing donor MHC are taken up by host dendritic cells
➝ donor MHC is presented into peptides which are presented by host MHC
➝ T cell response is generated to the peptide derived from the processed donor MHC

38
Q

What is a HSCT?

A

➝ haematopoietic stem cell transfer

39
Q

What is graft vs host disease?

A

➝ if the transplanted tissue is immune cells there is the risk of donor immune cells attacking the host

40
Q

What reduces graft vs host disease?

A

➝ Removing T cells from the transplant or suppressing their function

41
Q

What is graft vs leukaemia?

A

➝ Sometimes mismatch and donor leukocytes can be beneficial which removes the original leukemia

42
Q

What is essential to maintaining a non-autologous transplant?

A

➝ Immunosuppression

43
Q

What are the three categories of immunosuppressant?

A

➝ General immune inhibitors
➝ Cytotoxic (kill proliferating lymphocytes)
➝ inhibit T cell activation

44
Q

What is an example of general immune inhibitors?

A

➝ Corticosteroids

45
Q

What are three examples of cytotoxic drugs used in immunosuppression?

A

➝ Mycophenolic acid
➝ cyclophosphamide
➝ methotrexate

46
Q

What are three examples of drugs that inhibit T cell activation?

A

➝ Cyclosporin
➝ tacrolimus
➝ rapamycin

47
Q

How does cyclosporin work?

A

➝ inhibits IL-12 production

48
Q

How does mycophenolic acid work?

A

➝ Blocks lymphocyte proliferation through inhibition of DNA synthesis in T and B cells

49
Q

How does rapamycin work?

A

➝ Blocks lymphocyte proliferation by inhibiting IL-2 signalling

50
Q

How does anti IL-2 receptor antibody work?

A

➝ Inhibits T cell proliferation by blocking IL-2 binding

51
Q

How does anti CD3 monoclonal antibody work?

A

➝ depletes T cells by targeting them for destruction

52
Q

What is an example of a combination immunosuppressive regime?

A

1) steroids - prednisolone
2) cytotoxic
3) immunosuppressive specific

53
Q

What is an immediate risk for transplant patients?

A

➝ more susceptible to infection and malignancy such as CMV

54
Q

What can immunosuppressive drug toxicity lead to?

A

➝ organ failure

➝ e.g cyclosporin nephrotoxicity

55
Q

What is the microbiome involved in?

A

➝ regulating adaptive immune responses

56
Q

How can anti-cancer immune responses be improved?

A

➝ FMT (fecal matter transplant)

π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž (14 decks)

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