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Immunology > Transplant Immunology > Flashcards

Transplant Immunology Flashcards

1
Q

what is the primary reason for mortality after a transplant ?

A

immune response to graft leads to rejection

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2
Q

difference b/w orthotopic and heterotopic

A

orthotopic is transplanting cell/tissue to the same anatomical site
heterotopic is transplanting to a different site

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3
Q

what is the difference b/w and autologous graft, synergeneic graft, and allogenic graft ?

A

autologous is graft to and from same individual
synergeneic is a graft from genetically identical ind. (twin)
allogenic is from genetically different individual

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4
Q

what complications in transplants are the result of what type of graft ?

A

allogenic graft

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5
Q

A MHC (a) graft will _______ by an MHC (a) host, whereas a MHC (a) graft will _________ by an MHC (b) host

A
  • Not be rejected

- will be rejected

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6
Q

What is the difference b/w CD8 and CD4 T cells ?

A

CD8 - cytotoxic t cells, MHC I restricted

CD4 - helper t cells, MHC II restricted

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7
Q

what 3 things do T cells NEED to become effector T cells

A
  • recognize Ag
  • MHC activation
  • Costimulatory molecule activation
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8
Q

T cells can recognize an alloantigen 2 ways, what are they and how do they differ ?

A

1 - Direct - T cell receptor engages naked alloantigen

2 - Indirect - APC engulfs an alloantigen, processes it then presents it to T cells

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9
Q

Indirect alloantigen recognition is an example of ?

A

Cross presentation or cross priming

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10
Q

once a T cell recognizes an alloantigen either directly or indirectly, what occurs ?

A

T cell becomes activated

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11
Q

What are the 3 ways an allogeneic T cell can lead to graft rejection

A

1 - hyperacute rejection (w/in minutes to hours)
2 - acute rejection (about 1-2 weeks)
3 - chronic rejection (6 months)

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12
Q

what happens during hyperacute rejection ?

A

Pre-existing alloreactive Ab are present in recipient

-leads to activation of complement cascade = inflammation = thrombosis formation

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13
Q

what occurs during acute rejection ?

A

CD8 and CD4 (T cells) become activated leading to

  • Cytotoxic t cells lyse target
  • helper t cells activate B cells to produce Ab (and same thing happens as hyperacute rejection)
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14
Q

What happens in chronic graft rejection

A

survive for about 6 months, but eventually blood vessels thicken from increased growth factor production = occlusion of vessels = graft rejecetion

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15
Q

In order from best to least, which types of grafts are least likely to cause rejection

A

1 - autologous
2 - synergeneic
3 - allogenic

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16
Q

Besides prevention, what is another strategy that can be used to reduce the probablitlity of graft rejection

A

immunosupression via drugs

17
Q

There are 4 immunosupression drugs we need to know that prevent graft rejection, what are they ?

A

Rapamycin
Anti-CD3 monoclonal Ab
Anti-IL-2 receptor Ab
CTLA-4 Ig

18
Q

How does immunosupression drug rapamycin work

A

inhibits IL-2 signaling = No T cell proliferation

19
Q

how does immunosupression drug Anti CD3 monoclonal Ab work ?

A

depletes T cells by binding to CD3 = phagocytosis

20
Q

how does immunosupression drug Anti IL-2 receptor Ab work

A

inhibits IL-2 binding = No T cell proliferation

21
Q

how does immunosupression drug CTLA-4 Ig work ?

A

CTLA blocks co-stimulatory activation = no T cell activation (CTLA-4 doesnt allow CD28 to bind to B7)

22
Q

What are the 2 uses/ reasons for a bone marrow transplant

A

1 - treatment of hematological disesase

2 - restore an immune system destroyed by chemo/radiation

23
Q

what is the name of the disease, when the graft attacks the host in a bone marrow transplant ?

A

graft versus host disease

-hapens b/c trying to introduce a completely new immune system

24
Q

cells of what part of the immune system are Ag specific

A

adaptive immune system

25
Q

Some cancers downregulate MHC I, if this occurs what cells would become activated

A

NK cells, respond when no MHC is present

26
Q

Activated NK cells produce what important cytokine related to cancer immunology, what is the main function of this cytokine

A

IFN-gamma

-activates macrophages

27
Q

What are the 2 types of macrophages that affect cancer development

A

M1 macs - supress tumors

M2 macs - enhance tumors

28
Q

What distinguishes the function of what type of macrophage will be produced (M1 or M2) ?

A

cytokine microenvironment

29
Q

What cytokines lead to M1 macrophages

A

IFN-gamma

Good for fighting cancer

30
Q

what cytokines lead to M2 macrophages

A

IL-1, IL-4, IL-13

BAD for fighting off cancer

31
Q

Why are M2 macrophages bad for fighting off tumors ?

A

B/C they are healing/regenerative macs

-produce growth factors which inevitably enhance tumors

32
Q

what is the principal mechanism in tumor immunity, and how do these cells work ?

A

CD8 cytotoxic T cells
-once bind to Ag and become activated = they degranulate releasing perforin and granzyme B
-

33
Q

what is the diff. in function of perforin vs. granzyme B

A

perforin forms pore for granzme to enter target then granzyme induces apoptosis of target cell

34
Q

What are CD4 T cells potential roles in fighting off cancer ?

A

1 - Help activate CD8 T cells

2 - Prod. Th1 cytokines which lead to M1 macrophages (tumor supressors)

35
Q

What are B cells/Ab role in fighting off cancer ?

A

Some Ab can bind cancer cells = activates NK cells = degranulation = apoptosis

36
Q

Is there any way that an overexpression of the immune response can actually cause cancer ?

A

Yes, if to much inflammation you increase risk of cancer

37
Q

how does cancer increase the risk of cancer development

A

1 - Increase inflammation —-> increased cytokines
——> hyperplasia (increase cell proliferation) —–> dysplasia (abnormal cell dev.)
2 - Increase inflammation —-> increase free radicals damaging nucleic acids

Immunology (12 decks)

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