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Immunological Disorders > Lecture 8 - Transplant Immunology > Flashcards

Lecture 8 - Transplant Immunology Flashcards

1
Q

what are the three Transplant immunology tests?

A

HLA typing, HLA antibody screen and HLA crossmatch

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2
Q

what are the two types of transplants?

A

haematopoietic stem cells transplants and solid organ transplants

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3
Q

where do HSCs come from?

A

bone marrow, peripheral blood stem cells, umbilical cord

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4
Q

what complicates the use of composite tissue?

A

composite tissues contain intent donor immune effector cells which can cause GvH disease

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5
Q

what is pharmacogenetics?

A

associations with the HLA system and its response to therapeutic drugs

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6
Q

what is an example of pharmacogenetic associations?

A

HLA B57 disproportionally present with hypersensitivity to abacavir

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7
Q

what is HLA antigen typing?

A

profiling of the HLA present on patient/donor cells

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8
Q

what is HLA antibody screening?

A

detection and identification of anti-HLA formed in the patient

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9
Q

what is HLA crossmatching?

A

testing compatibility of patient HLA antibody profile against the donor, use recipients serum against cells from the donor

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10
Q

what is an autograft?

A

transplant on the same person

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11
Q

what is an allograft?

A

transplant of tissue or organ between two genetically non-identical members of the same species

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12
Q

what is an isograft?

A

transplant of tissue or organs between genetically identical members of the same species

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13
Q

what is a xenograft?

A

transplant between two different species

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14
Q

what are the issues in the process of transplantation?

A

complexity, preparation, conditioning, cost

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15
Q

what are the issues in the patient aspect of transplantation?

A

has to be in optimum condition, disease needs to be controlled

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16
Q

what are the complications of the transplant process?

A

infection due to immunosuppressants, rejection due to immune response, GVHS, relapse or a secondary disease

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17
Q

what is an example of a secondary disease caused by a transplant?

A

aggressive treatment used to rid of one disease can lead to another, e.g. different types of leukaemia

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18
Q

what are the challenges or transplants?

A

availability of an organ, donor selection process, immunosuppression can be fatal

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19
Q

what is HLA in relation to MHC?

A

HLA are antigens of the MHC located on chromosome 6

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20
Q

what is HLA class I?

A

HLA genes A, B and C

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21
Q

what is the structure of HLA class I?

A

single transmembrane alpha chain, covalently linked to polymorphic beta 2 macroglobulin

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22
Q

what is class II HLA?

A

HLA DR, DQ and DP

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23
Q

what is the structure of HLA class II?

A

2 transmembrane chains

24
Q

what size peptides bind to class I?

A

8 or 9 amino acids

25
Q

where do peptides bind on class I?

A

in area between helices and beta sheet

26
Q

what does variation in beta sheet cause?

A

a more varied range in the peptides that can bind

27
Q

what does variation in helices cause?

A

this determines which T cell receptors can bind to the HLA

28
Q

what size peptides bind to class II HLA?

A

14-21 amino acids

29
Q

what differs between class I and I?

A

tissue distribution

30
Q

where is class I expressed?

A

on all somatic cells

31
Q

where is class I not expressed?

A

CNS neurones, corneal endothelium, exocrine portion of pancreas

32
Q

what does class I present peptides to?

A

CD8 T cells

33
Q

where is class II expressed?

A

B cells, monocytes, macrophages, dendritic cells

34
Q

what does class II present peptides to?

A

CD4 T cells

35
Q

why are HLA genes inherited as a group?

A

close together on chromosome 6 and so do not undergo genetic variation

36
Q

what fields are needed for HLA matching?

A

1 and 2

37
Q

why is HLA most important group in transplants?

A

highest polymorphism, primary non-self target of immune system, decreases rejection when matched

38
Q

how is hyperacute rejection caused?

A

by pre-existing anti-HLA antibodies in the host, leading to complement activation and IV coagulation

39
Q

how does hyper acute rejection cause loss of the graft?

A

complement activated, capillaries become blocked and inflammation causes necrosis leading to loss

40
Q

how is accelerated graft rejection caused?

A

by pre-sensitisation of the donor to HLA via a transfusion or pregnancy causing memory leading to humeral or cellular response

41
Q

how is acute graft rejection caused?

A

by HLA mismatches causing a cellular immune response

42
Q

which type of rejection is most common?

A

acute

43
Q

how long does hyper acute rejection take?

A

minutes or hours

44
Q

how long does accelerated rejection take?

A

within 3 days

45
Q

how long does acute rejection take?

A

1 to 3 weeks

46
Q

how is acute rejection prevented?

A

immunosuppression and plasmaphoresis

47
Q

how is chronic graft rejection caused?

A

either a prolonged series of acute rejection tasks or possible slow progressive inflammatory response

48
Q

how is chronic rejection characterised?

A

by graft arterial occlusions known as graft arteriosclerosis

49
Q

what does chronic rejection lead to?

A

ishcemia and cell death

50
Q

what is the major cause of allograft rejection?

A

antibody mediated rejection

51
Q

how is antibody mediated rejection caused?

A

pre-formed antibodies or de-novo antibodies formed due to transplant

52
Q

how does antibody mediated rejection lead to loss of graft?

A

complement activated, leucocytes recruited and NK/monocyte mediated cytotoxicity occurs leading to endothelial damage and loss of vascular integrity

53
Q

how is antibody mediated rejection diagnosed?

A

impaired renal function, histological evidence of Ab activity such as C4d deposition, detection of HLA antibodies

54
Q

what is the treatment of antibody mediated rejection?

A

removal of antibodies via plasmapheresis, immunoadsorption or IV IgG

55
Q

how does IV IgG suppress an immune response?

A

inhibits T cell proliferation, cytokines and complement

Immunological Disorders (8 decks)

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