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Block 6 Week 2 > Transplant Immunology > Flashcards

Transplant Immunology Flashcards

1
Q

(blank) has evolved as the treatment of choice for end-stage organ failure resulting from a wide variety of causes

A

transpant

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2
Q

Transplant of which organs are commonplace?

A

kidney, liver, pancreas, intestine, heart and lung

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3
Q

The main problem facing the field today is not surgical technique, or management of rejection or complications, but rather (blank)

A

supply of organs

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4
Q

The number of transplants has not kept pace with the steadily growing waiting list due to (blank)

A

(ethical dilemmas)

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5
Q

What does allogenic mean?

A

genetically different within the same species

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6
Q

What makes me different from you?

A

alloantigens

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7
Q

Transplanted tissues (grafts) between genetically different (allogeneic) individuals are attacked by the (blank)

A

immune response (like pathogens)

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8
Q

Antigenic differences between individuals (alloantigens) induce (blank) immune responses

A

alloreactive

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9
Q

The most important alloantigens are (blank) protens

A

MHC (has a major number of alleles)

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10
Q

Which of the MHC molecules would be more problematic in tissue transplant?

A

MHC class I (because they are found on all cells)

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11
Q

The MHC gene complex in humans is called (blank)

A

human leukocyte antigen (HLA)

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12
Q

What someones HLAs are, are called (blank)

A

HLA typing

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13
Q

HLA MHC class I are found at what loci?

A

A B C

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14
Q

HLA MHC class II are found at what loci?

A

DR, DQ, DP

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15
Q

The HLA complex is located at chromosome (blank)

A

6

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16
Q

Every human expresses (blank) MHC class I alleles (one allele of HLA-A, -B, and -C from each parent) and at least six MHC class II alleles (one allele of HLA-DQ and -DP and one or two of -DR from each parent

A

6

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17
Q

WHat principle is this:

several MHC genes in the genome

A

polygenic

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18
Q

What priniciple is this:

each gene has a large number of aleles

A

polymorphic

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19
Q

(blank) have the most allels of any loci in the human genome

A

MHC

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20
Q

(blank) means that both alleles on matching chromosomes will be expressed on the cell surface

A

co-domnance

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21
Q

T or F
It is unlikely that two individuals would have the same MHC haplotype (alleles on a chromosome), except in the case of monozygotic (identical) twins

A

T

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22
Q

How can you get a successfull transplant?

A

If you transplant tissue from one part of your body to another part of your body (autograft) or between genetically identical humans (syngeneic graft)

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23
Q

What is syngeneic graft?

A

getting tissue from a genetically identical human

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24
Q

Allogenic transplants (allografts i.e transplant from someone else) are rejected in about (blank) days after grafting

A

10-13 days

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25
Q

Transplans b/w individuals of different species (xenogeneic) are also rejected rapidly. What are thes grafts called?

A

xenografts

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26
Q

In allografts and xenografts the rapid death of the transplanted tissue is called (Blank)

A

acute rejection

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27
Q

If you differ in just one MHC allele can you transplant the organ?

A

nope it still will cause rejection

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28
Q

What was the earliest tissue transplant and most common?

A

Blood transfusion

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29
Q

Why are RBC and Platelets pretty easy to transplant?

A

because they have a very small amoutn of MHC and usually are not targets of T cells

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30
Q

What must you match on blood cells to transfuse?

A

Blood must be matched for ABO and Rh blood group antiges to avoid rapid destruction by antibodies in the recipient

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31
Q

Grafts between MHC allogeneic mice are rejected in 10-13 days. What happens if you put a second graft in the same animal? What does this tell us?

A

it is rejected even faster

Second-set rejection reveals immunological memory.

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32
Q

IF you take a sensitized animal (i.e one that already had been given a tissue and rejected it) and take the animals T cells out of it and then transfer it to a naive animal what will happen?

A

it will have immunological memory and respond super bad to a tissue transplant, as if the first mouse was give a second transplant

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33
Q

Matching MHC types between donor and recipient prolongs but does not (blank) graft rejection

A

eliminate

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34
Q

Do MHC-matched human siblings have successful transplantation? WHy?

A

Cuz there are still other differences that will still elicit an immune response

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35
Q

What is direct allorecognition?

A

activated APC from donor graft migrate to lymphoid organ. APC presents a donor peptide to recipient T cell along with co-stimulation (CD80/86) which will elicit immune response and rejection

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36
Q

What cell will cause graft destruction first?

A

CD8 T cells

37
Q

WHat is indirect allorecognition?

A

Your own APC cells present the graft peptide as a foreigner and elicits T cell response

38
Q

What are the clincal manifestations of hyperacute graft rejection?
Why does this happen?

A

occurs w/in minutes of transplant and has thrombosis of graft vessels and ischemic necrosis of graft
Recipient antibodies attack RBCs in the grafted tissue via complement and clottign system. (this is rare cuz now we test for blood type and for antibodies against the cells of potential donor)

39
Q

What does a graft need to be successful?

A

needs a blood supply

40
Q

What is this:
normal kidney grafted into patient with defective kidney and preexisitng antibodies aganst donor antigens. Antibodies against donor antigens bind vascular endothelim of graft initiating an inflammatory reponse which occludes blood vessels and graft becomes engorged and purple colored because of hemorrhage.

A

Antibody-mediated hyperacute graft rejection

41
Q

What is acute graft rejection?

How do you avoid this?

A

happens within days/weeks after transplant, principle cause of early graft failure, mediated by CD8 T cells (MAJOR), complement and antibodies

Immunosuppresive therapy,,

42
Q

In acute graft rejection, recipient (blank) cells attack alloantigenic MHC peptides in the graft

A

CD8 T

43
Q

What is chronic graft rejection?

A

Insidious (slowly but hurtfully) form of graft damage that occurs over months to years, leads to loss of graft function.

44
Q

How does chronic graft rejection present?

A

as graft fibrosis and narrowing of graft blood vessels (graft arteriosclerosis) caused by CD4 T cells that are perpetually releasing mediators

45
Q

In chronic graft rejection, (bank) react with graft alloantigens and secretecytokines that stimulate the proliferation and activities of fibroblasts and vascular smooth muscle cells

A

CD 4 T cells

46
Q

What is the principal cause of graft failure?

A

Chronic graft rejection

47
Q

Where do you see the fibrosis and scarring of chronic graft rejection?

A
  • Heart (accelerated coronary artery atherosclerosis)
  • Lung (bronchiolitis obliterans)
  • Liver (vanishing bile duct syndrome)
  • Kidney (chronic allograft nephropathy)
48
Q

What factors increase risk of chronic rejection?

A

previous episode of acute rejection
inadequate immunosuppression
Donor-related factors (e.g old age, hypertension)
Long cold ischemia time; reperfusion injury to organ
Recipient-related factors (e.g, diabetes, hypertension, hyperlipidemia)
Post-transplant infection (e.g. CMV)

49
Q

(blank)is used to correct hematopoietic defects or to restore bone marrow cells damaged by irradiation or cancer chemotherapy

A

Hematopoietic stem cell transplantation

50
Q

Is bone marrow easy to transplant?

A

no, Allogeneic bone marrow cells are very immunogenic, so that successful transplantation requires careful HLA matching of donor and recipient

51
Q

Mature allogeneic T cells in the graft can attack the recipient’s tissues, resulting in a serious clinical reaction called (blank)

A

graft-versus-host disease

52
Q

WHy do peope use myeloablative therapy (kills patients bone marrow)?

A

to destroy messed up bone marrow or make room for donor bone marrow to fit

53
Q

What is super scary about bone marrow transplants?

A

mature donor T cells attack recipient tissues causing graft versus host disease due to alloantigens on the bone marrow :(

54
Q

Can you give a scid kid a bone marrow transplant?

A

yes!!! because skid kids dont have functioning T cells so nothing will attack the donor bone marrow

55
Q

When you have graft vs host disease what are the symptoms?

How do you control this?

A

you see a rash on the face and diarrhea, pneumonitis and liver damage :(
immunosuppressive drugs

56
Q

What is the graft vs leukemia effect?

A

the donor T cells attack the cancerous cells in leukemia

57
Q

What doesnt the trophoblast have? WHat does this mean?

A

MHC molecules

That T cells from mom wont recognize MHC molecules from dad inside the fetus

58
Q

Tryptophan is essential for (blank) function

A

T cell

59
Q

What keeps moms T cells from attacking the placenta?

A

the placenta secretes indole amine dioxygenase that catabolizes tryptophan and starves T cells (tryptophan is essential for T cell function)

60
Q

Placental secretion of (blank) causes immune deviation

A

cytokines

61
Q

T or F
With the extremely rare exception of grafts between identical twins, all recipients of tissue transplants will require immunosuppressive drug treatment for life

A

T

62
Q

T or F

Too little immunosuppression, their grafts will be rejected; too much immunosuppression, they will die from infections

A

T

63
Q

Tissue transplants are rejected by the immune system, and the major antigen targets of rejection are (blank)

A

MHC molecules

64
Q

The mainstay of preventing and treating the rejection of organ transplants is (blank)

A

immunosuppression

65
Q

The most useful immunosuppressive drug in clinical transplantation is(blanK). What does it do?

A

cyclosporin A
perfers to stop T cells from dividing via blocakage of T cell phosphatese calcineurin and prevents transcription factor NFAT from activating cytokine genes

66
Q

What does corticosteroids do?

A

inhibit inflammation, shut off NFKb, inhibits cytokine production by macrophages.

67
Q

What does Azathioprine, cyclophosphamide, mycophenolate do?

A

inhibit proliferation of lymphocytes by interfering with DNA synthesis

68
Q

What does Cyclosporin A, tacrolimus (FK506) do?

A

inhibits calcineurin-dependent activation of NFAT; block IL-2 production and proliferation by T cells

69
Q

What does rapamycin (sirolimus) do?

A

inhibits proliferation of effector T cells by blocking Rictor-dependent mTOR activation

70
Q

What does Fingolimod do?

A

blocks lymphocyte trafficking out of lymphoid tissues by interfering with signaling by the sphingosine-1-phosphate receptor

71
Q

Why dont you want to use long term corticosteroid?

A

because they have a lot of bad side effects

72
Q

What crosses nuclear membrane to bin to NF-Kb promotor and inhibits its transcription to reduce cytokines?

A

corticosteroids

73
Q

What down-regulates proinflammatory cytokines, NO, prostaglandins, leukotrienes, and adhesion molecules?

A

corticosteroids

74
Q

What are the three most common cytotoxic drugs/immunosuppressive agents?
How do they work?

A

azathioprine, mycphenolate, cyclophosphamide
they block DNA syntehsis and kill dividing cells (includes tumor cells and lymphocytes)

lots of bad side effects**

75
Q

What can CD4 T cells do to mess someone up pretty bad?

A

releases cytokines that can cause inflammation and fibrosis

76
Q

What is the effect of corticosteroids on cytokines?

which cytokines in particular?

A

decreases them

IL-1, TNF-alpha, GM-CSF, IL-3, IL-4, IL-5, CXCL8

77
Q

What is corticosteroids effect on NOS?

A

decreases it so you have decreased NO

78
Q

What is corticosteroids effect on phospholipase A2, Cyclooxygenase type 2, annexin-1?
What does this result in?

A

decreases phospholipase A2 and cyclooxygenase type 2
increases annexin-1

Decrease prostaglandins and leukotrienes

79
Q

WHat wil be corcticosteroids effect on adhesion molecules? what will this result in?

A

decrease, reduced emigration of leukocytes from vessels

80
Q

What will corticosteroids do to endonucleases? What wil this result in?

A

increase it

induction of apoptosis in lymphocytes and eosinophils

81
Q

Microbial inhibitors of T cell signaling are used to prevent (blank)

A

allograft rejection

82
Q

What are the three most common microbial inhibitors of T cell signaling?

A

cyclosporin A, Tacrolimus, and Rapamycin

83
Q

How does Cyclosporin A, Tacrolimus (FK506), and Rapamycin (Sirolimus)
work?

A

they bind to intracellular immunophilins to inhibit T and B cell proliferation and granulocyte function, but affect immune responses indiscriminately.

84
Q

Explain in detail the mode of action of cyclosporin A?

A

A T cell internalize calcium whih will bin to calmoduling which will then activate calcineurin. Calcineurin is what causes activation NFATvia dephosphorylation to make IL-2 and have T Cells proliferate. Cyclosporin A will inhibit calcinerin and prevent the dephosphorylation of NFAT. This does not have a lot of side effects

85
Q

What does RAPTOR and mTOR do and what can block this and work as an immunosuppressent?

A

it causes T cell proliferation

Sirolimus (rapamycin)

86
Q

(blank) can be used to prevent graft rejection

A

monoclonal antibodies

87
Q

How does Muromomab (OKT3) work?

A

it is an anti-CD3 so blocks all T cell production

88
Q

Ho does Daclizumab and Basiliximab work?

A

it is an anti-IL2 receptor that will inhibit the proliferation and differention of T cells

Block 6 Week 2 (7 decks)

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