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Immuno > Transplantation > Flashcards

Transplantation Flashcards

1
Q

What is an autologus graft (isograft)?

A

a graft transplanted from an individual to the same individual

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2
Q

What is a syngeneic graft?

A

a transplant between two genetically identical individuals

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3
Q

What is an allogeneic graft?

A

a transplant between two genetically dissimilar individuals of the same species

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4
Q

What is a xenogeneic graft?

A

a transplant between members of two different species

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5
Q

What are orthotopic grafts?

A

is a graft that is placed in its normal anatomic location

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6
Q

What is a heterotropic graft?

A

A transplant placed in an anatomically different site

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7
Q

What are first and second set rejections?

A

Basically first and second immune responses to grafts

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8
Q

What are immunologicall privileged sites?

A

locations in the body where an allogeneic transplant can be placed without risk of rejection

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9
Q

What are the three reasons for immunologically privileged sites?

A
  1. Extracellular fluid does not leave through lymph system
  2. TGF-beta released at these sites
  3. Fas ligand expressed on cells to induce T cell apoptosis
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10
Q

What is Sympathetic ophthalmia?

A

an eye disease that occurs when one eye is damaged by trauma and an autoimmune response to eye proteins ensues to threaten the undamaged eye

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11
Q

Are transplants between identical twins ever rejected?

A

Rarely

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12
Q

Are transplants between genetically dissimilar individuals rejected?

A

Almost always

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13
Q

Can children give grafts to parents or vice versa?

A

No

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14
Q

What are the molecules that are being rejected in grafts?

A

MHC class I and II

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15
Q

How fast do hyperacute rejections take place? What is the mechanism behind this?

A

within minutes, due to complement being activated by memory antibodies, and causing thrombosis

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16
Q

What are examples of hyperacute rejections?

A

Incorrect blood transfusions

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17
Q

How long do acute rejections take to develop?

A

1 month

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18
Q

What are the two mechanisms behind acute rejection?

A
  1. Acute humoral rejection d/t antibody and complement mediated lysis of graft tissue
  2. Acute cellular rejection caused by cell mediated lysis by CTLs
19
Q

What is the treatment for acute rejections?

A

increased immunosuppression such as high dose steroid therapy or anti-T cell antibodies

20
Q

How long does chronic rejection take place?

A

Over months / years

21
Q

What is the pathogenesis of chronic rejection?

A

Not totally known, but there are fibrotic changes in the graft

22
Q

What is the pathogenesis of graft rejection?

A

Host APCs present MHC proteins of graft as foreign molecules via the class II pathway.

23
Q

How are CTLs activated against grafts, if the grafts do not have self MHC cells?

A

T cells recognize self peptide with foreign MHC. Basically fools T cells.

24
Q

True or false: either dendritic cells from the donor (direct) or recipient (indirect) can be used to activate graft rejection

A

True

25
Q

What are the three means through which grafts are destroyed in the acute rejection?

A
  1. CD8+ CTLs lyse graft cells
  2. CD4+ T cells recruit macrophages
  3. Alloantibodies activate complement
26
Q

What are minor histocompatability antigens?

A

none MHC factors that may generate an immune response

27
Q

What happens after dendritic cells present MHC molecules to host T cells?

A

CD4+ Th cells prodive IL-2 and IFN-gamma to activate CD8 T cells to produce CTLs

28
Q

What are the three strategies used to reduce graft rejection?

A
  1. Select compatible graft
  2. Immunosuppression
  3. Deplete passenger leukocytes from graft
29
Q

What is the effect of corticosteroids?

A

Lyse immature thymocytes, block release of cytokines from macrophages, inhibit leukocyte migration

30
Q

What is the mech of action of cyclosporine?

A

Inhibits IL-2 and IFN-gamma

31
Q

What is the major drawbacks of cyclosporin?

A

It’s nephrotoxic

32
Q

What is anti-lymphocyte globulin and how does it work?

A

Horse immunogloin against human lymphocytes. Kills all human lymphocytes to prolong graft

33
Q

What is graft-versus-host disease?

A

When bone marrow cells attack the rest of the body

34
Q

What causes acute GVHD?

A

mature T cells responding to host alloantigens.

35
Q

How can you remove the T cells from bone marrow transplants?

A

in vitro treatment with anti-CD3 monoclonal antibodies (along with Complement)

36
Q

Why would you want to have some variation in HLA type for leukemia pts?

A

To kill CA

37
Q

What is the chemical given to bone marrow donors to increase stem cells/ spill into blood?

A

Granulocyte colony-stimulating factor (G-CSF)

38
Q

What are the three major mechanisms that prevent a mother’s body from killing a fetus?

A
  1. Trophoblasts cells do not express paternal MHC proteins
  2. Trophoblast cells secrete TGF-beta
  3. Y is broken down at fetal-materal interface, diabling T lymphocytes
39
Q

Why does the liver carry an increased risk of GVHD?

A

Has a lot of donor lymphocytes

40
Q

What is the function of HLA-G expressed by fetal trophoblast cells?

A

Inhibits NK cells

41
Q

What are the three steps involved in the activation of CTLs against a graft?

A
  1. Dendritic cells present antigen to CD4+ T cells
  2. CD4+ T cells release IL-2 and IFN-gamma to stimulate CTLs.
  3. CTLs kill via CD8+/MHC I graft cells
42
Q

What is the difference between direct and indirect stimulation of T cells in graft rejection?

A

Direct = using donor’s dendritic cells

Indirect = using recipients dendritic cells

43
Q

What is the mechanism of action for cyclosporine?

A

Inhibits the expression of IL-2 and IFN-gamma, preventing CTL formation.

44
Q

Cyclosporine is not good at inhibiting secondary immune responses. What is the effect of this?

A

Pts retains ability to fight off infections that he/she has already been exposed to.

Immuno (16 decks)

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