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Immunology 4 > Transplantation and tumor > Flashcards

Transplantation and tumor Flashcards

exam 4

1
Q

one person to the same person

A

autograft

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2
Q

person to a genetically identical recipient

A

syngraft

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3
Q

person to a genetically different recipient

A

allograft

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4
Q

graft to a different species

A

xenograft

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5
Q

minutes or hours

A

hyperacute rejection

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6
Q

due to preformed ab in the recipient

A

hyperacute rejection

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7
Q

10-14 days

A

acute rejection

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8
Q

due mainly to cell mediated immunity but some injury is also antibody mediated

A

acute rejection

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9
Q

months or years after the transplant

A

chronic rejection

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10
Q

Due to ab, T-cell and NK cell attack on the graft

A

chronic rejection

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11
Q

mechanism of acute allograft rejection,

direct contact between _____ and the graft

A

CD8+

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12
Q

mechanism of acute allograft rejection,

inflammation, macrophage activation, infiltration of phagocytic cells

A

locally released cytokines and chemokines

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13
Q

mechanism of acute allograft rejection, complement binding and ADCC (ab dependent cellular cytotocicity by NK cells

A

Ab against donor HLA

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14
Q

mechanism of acute allograft rejection,

direct

A

NK cell attack

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15
Q

Stem cells can be obtained from the _____________ (after treatment with colony stimulating factors) or from ____________ blood or from ____________.

A

Stem cells can be obtained from the peripheral blood (after treatment with colony stimulating factors) or from umbilical cord blood or from bone marrow.

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16
Q

The major danger of bone marrow transplantation

A

competent T-cells from the donor may be transplantated giving rise to graft versus host disease

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17
Q

a reaction of donor T-cells against recipient MHC

A

graft versus host disease

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18
Q

For a GVH to occur: [3]

A
  1. graft must contain live T-cells
  2. recipient must be immunosuppressed
  3. donor and recipient must have different HLA types
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19
Q

CD4+ T cells in the graft are activated by allogeneic molecules and produce a ______________

A

“cytokine storm”

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20
Q

cytokine storms recruits __________, ____________ and ____________ to create the severe inflammation characteristic of GVH

A

other T cells, macrophages and NK cells

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21
Q

acute GVHD rash that characteristically involves

A

palms and soles

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22
Q

when a kidney is transplanted the __________ T cells attack the transplant

A

recipient

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23
Q

When the bone marrow is transplanted the T cells in the ________ attack the recipient tissues

A

transplant

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24
Q

recipient T cells attack

A

transplant rejection

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25
Q

T cells in the transplant attack

A

Graft versus host disease

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26
Q

block a T-cell phosphatase and inhibit cytokine production and that serves as a immunosuppressive Drugs

A

cyclosporine and FK506

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27
Q

calcineurin

A

T-cell phosphatase that inhibits cytokine production

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28
Q

inhibit cytokine production and are anti-inflammatory and that serves as a immunosuppressive Drugs

A

corticosteroids

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29
Q

monoclonal antibody that serves as a immunosuppressive Drugs

A

Anti-CD3

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30
Q

antibody that serves as a immunosuppressive Drugs

A

Anti-IL-2 receptor

31
Q

no b-cell involvement

A

GVH

32
Q

problem with all forms of immunosuppressive therapy

A

normal immune response sagainst microorganisms are reduced giving rise to an increased incidence of infection

33
Q

candida

A

fungi

34
Q

pox and herpes viruses

A

large viruses

35
Q

mycobacterium tuberculosis

A

intracellular bacteria

36
Q

toxoplasma

A

intracellular parasites

37
Q

tumor express a variety of tumor antigens that can be recognized by the immune system

A

tumor immunology

38
Q

types of antigens on the surface of tumor cells [5]

A
  1. virally controlled antigens
  2. oncofetal antigens
  3. mutant antigens
  4. abnormal peptides made by tumor cells
  5. tissue specific differentiation antigens
39
Q

primary hepatocellular carcinoma

A

alpha-fetoprotein

40
Q

colon carcinoma

A

carcino-embryonic antigen

41
Q

alpha-fetoprotein and CEA- carcino-embryonic antigen

A

oncofetal antigens

42
Q

PSA (prostate-specific antigen), B-cell (CD19, CD20) and T-cell markers (CD3, CD4 or CD8)

A

Tissue specific differentiation antigens

43
Q

Her2/neu

A

mutatn antigens

44
Q

fetal liver

A

alpha-fetoprotein

45
Q

Her2/neu found on breast cancer can be tx. with

A

Herceptin

46
Q

PSA

A

prostate-specific antigen

47
Q

all kappa or all lambda?

A

lymphoma

48
Q

changes on the surface of malignant cells that can occurs?

A

tumors may lose HLA class 1

49
Q

tumors that have lost HLA class I ____________ but thwy will be killed by

A

will not be killed by CD8+ cells and NK cells that recognize and are cytotoxic to HLA Class I negative cells

50
Q

large granuloar lymphocytes and destroy infected and malignant cell that have absent or defective MHC I

A

NK cells

51
Q

NK cells have __ receptors that can bind to ______ resulting in ADCC

A

NK cells have Fc receptors that can bind to IgG resulting in ADCC

52
Q

NK cells can be activated by

A

cytokines” IL-2, IL-12 and IFN gamma

53
Q

NK cells produce

A

variety of cytokines

54
Q

Principal immune mechanism of killing tumor cells is by

A

cytotoxic CD28 cells

55
Q

killing of tumor cells can also take place by

A

activated macrophages and by NK cells

56
Q

How do tumors escape?

A

1) They release immunosuppressive factors e.g. IL-10 and TGF-beta
2) They release factors that activate TREG cells
3) They select antigen-negative variants
4) They upregulate the expression of immune checkpoint molecules such as PD-1 and PD ligand 1 (PD-L1)

57
Q

cytotoxic CD8 cells kill by

A

using granzyme and perforin, and expression of FasL on the CD8 cell

58
Q

Cancer immunotherapy [5]

A

1) Immunization against oncogenic viruses
2) Stimulation of innate immune mechanisms
3) Checkpoint inhibitors
4) CAR T-cells
5) Monoclonal antibodies

59
Q

1) Immunization against oncogenic viruses

A

Hep B and HPV

60
Q

Stimulation of innate immune mechanisms [2]

A
  1. Imiquimod activates a Toll like receptor (TLR7)

2. BCG produces inflammation in bladder wall

61
Q

checkpoint inhibitors

A

block CTLA-4 or the PD-1/PDL-1 interaction to remove the “brakes” from cytotoxic T-cells

62
Q

magic bullets –immunotoxins

A

monoclonal antibodies

63
Q

risks of blocking CTLA-4 or PD-1:

A

autoimmune reactions

64
Q

less severe autoimmune reactions is with an

A

anti-PD1 antibody

65
Q

are monoclonal antibodies attached to toxins such as ricin or radioactive isotopes.

A

immunotoxins

66
Q

These are delivered specifically to the malignant cells to initiate direct killing.

A

immunotoxins

67
Q

targets CD20 on B-cell lymphomas

A

Rituximab

68
Q

targets growth factor receptors in colon cancer

A

Erbitux

69
Q

(anti Her2/Neu) blocks growth factor signaling

A

Herceptin

70
Q

Mechanisms of MAb-mediated killing, [3]

A
  1. complement-mediated lysis and phagocytosis
  2. attach by macrophages or NK cells
  3. signaling, leading to apoptosis or growth arrest
71
Q

monoclonal Ab where one arm binds to CD3 and the other to CEA

A

bispecific T cell engagers

72
Q

CEA-CD3

A

T-cell bispecific Ab

73
Q

designed to redirect T cells to tumor cells by simultaneously binding to CD3 found on T cells and CEA, a tumor surface antigen

A

CEA-CD3 TCB

Immunology 4 (9 decks)

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