Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Transplantation and Immunosuppression > Flashcards

Transplantation and Immunosuppression Flashcards

1
Q

Autograft

A

from one part of the body to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Isograft

A

between genetically identical twins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Allograft

A

between different members of the same species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Xenograft

A

between different species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sir Peter Medawar (Nobel prize 1960)

A

“Graft rejection is an adaptive immune response”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Skin transplant rejection

A
  • mediated by lymphocytes
  • specific response
  • escalating intensity with exposure
  • demonstrates memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What graft specific antigens are targeted?

A
  • MHC (class I&II)
  • class I present CD8+ T cells (on all nucleated cells(
  • class II present to CD4+ Tcells (restricted to DC, macrophages, Bcells etc)-APCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MHC are polymorphic

A

HLA - human leukocyte antigen

-polymorphic therefore an exact match is unlikely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Human MHC is located on which chromosome?

A

chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Serologic HLA testing

-less common now in era of molecular HLA testing

A
  • uses antibodies specific for different HLA alleles
  • bind to cells ecpressing specific HLA
  • detect bound antibody by ability of complement to lyse the cells
  • lysed cells take up dye
  • can therefore map donor/recipient HLA alleles and optimise compatibility of transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How would you determine if a patient has any pre-formed antibodies to the donor (HLA) :Cytotoxic cross mathing

A
  1. cells (T and B separated) from the potential donor
  2. patient serum added
  3. complement added
  4. no antibody binding to cells, cels are not killed by complement action (live cells stain green)
  5. patient has HLA antibody that binds to HLA antigen on cells in well, causing cells to be killed by complement action (stained red)
  6. Add stain to distinguish live and dead cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Allorecognition: INDIRECT

A
  • uptake of allongenic antigen by host APC
  • donor antigen degraded into peptides and presented on recipient MHC as for any exogenous antigen
  • activated T cells can provide help to effector cells (Macrophages, antigen specific Bcells etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Allorecognition: DIRECT

A
  • donor APC (passenger leukocytes) can leave the graft and migrate to the draining lymph node
  • appropriate TCRs can directly recognise aloo-MHC as foreign (a mixed lymphocyte reaction;MLR)
  • T cells are strongly activated, and drive effector responses
  • important in early response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stages of graft rejection:

A
  • hyperacute
  • acute
  • chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hyperacute:

A
  • usually requires sensitisation/Ab formation
  • less prominent in first allografts
  • Ab and complement mediated
  • occurs following vascularisation (minutes to hours)
  • look over stages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute transplant rejection:

A
  • cellular response to graft, involving CD4 and CD* Tcells and effectors (macrophages via IFNg/TNF))
  • help B cells(via IL-4)
  • rapid
  • can start about a week after transplant
  • occurs most often within the first year
17
Q

Chronic transplant rejection

A
  • slowly progressive, long term loss of function (after 1 year)
  • associated with low grade chronic DTH, fibrosis, vascular pathology
18
Q

Corticosteroids

A
  • powerful anti-inflammatory drugs
  • bind to steroid receptors in cell cytoplasm
  • affect gene transcription (prevent production of cytokines IL-1,IL-3,IL-4, TNF, GM-CSF)
  • block prostaglandin production
  • reduce cell migration
  • promotes inflammatory cell apoptosis
19
Q

Nucleotide synthesis inhibitors

A
  • azothioprine and mycophenolate mofetil (MPA)
  • blocks purines synthesis
  • inhibits DNA and RNA synthesis
  • prevents lymphocyte division
  • prevents IL-2 production and lymphocyte activation
  • toxicity to other dividing cells
20
Q

Calcineurin Inhibitors

A
  • cyclosporin revolutionised kidney transplantation in the 80s
  • complexes with calcineurin to prevent NFAT de-phosphorylation
  • NFAT can’t induce IL-2 gene transcription
21
Q

Cytokine action inhibitors

A
  • rapamycin (sirolimus)
  • blocks mTOR(mammalian target of raamycin)
  • prevents cell cycle (g1->S)
22
Q

Biologic agents (antibodies and fusion proteins)

A
  • Anti CD3 (OKT3)
  • disables CD3 receptor
  • Anti IL-2 receptor (CD25)
23
Q

Side effects of these immunosuppresants

A
  • corticosteroids (growth retardation, osteoporosis, hypertension, obesity diabetes)
  • Nucleotide synthesis inhibitors (bone marrow suppression, hepatic dysfunction, hair loss, GI effects)
  • Calcineurin inhibitors (diabetes etc)
  • Antibodies (cytokine release syndrome etc)
24
Q

what is donor specific tolerance?

A
  • introduced to the recipient
  • research ongoing
  • avoids long term treatment with broad acting immunosuppressants
25
Q

Self tolerance

A
  • control or removal of T cells specific for innocuous or self antigens
  • active processes include: regulation/suppression, anergy, apoptosis

Immunology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions