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Defence > TID > Flashcards

TID Flashcards

1
Q

What was the first transplanted material?

A

→cornea

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2
Q

What is the difference between autologous and syngeneic donor relationships?

A 
→autologous= within same individual
→syngeneic= donor with a genetically identical
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3
Q

What is allogenic transplant?

A

→Donors and recipients are from the same species but genetically different

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4
Q

What is xenogeneic transplant?

A

→Donor and recipient are different species

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5
Q

What are immune responses to transplant mainly due to?

A

→differences the antigens forming the major histocompatibility complex

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6
Q

Where are HLA genes found?

A

→chromosome 6

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7
Q

What may be foreign in transplants?

A

→both the MHC protein and the peptide in its binding groove may be foreign

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8
Q

What is the outcome of indirect allorecognition of self HLA and non-self peptide?

A

→Tcell activation

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9
Q

What is the outcome of direct allo-recognition of non-self HLA in a donor cell?

A

→Unmatched HLA + peptide = T-cell activation

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10
Q

What needs to be matched to reduce likelihood of problems with transplants?

A

→match 4/6 MHC class II loci

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11
Q

Compare live and dead donors

A

→Organs from deceased donors are also likely to be in inflamed condition due to ischemia

→Transplant success is less sensitive to MHC mismatch for live donors

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12
Q

What are the types pf graft rejections?

A

→Hyperacute rejection

→Acute rejection

→Chronic rejection

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13
Q

When does hyperacute rejection occur?

A

→Within a few hours of transplant

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14
Q

What type of transplants commonly see hyperacute rejection?

A

→highly vascularised organs (e.g. kidney)

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15
Q

What is the blood group implicated in hyperacute rejection?

A

→ABO

→MHC-I

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16
Q

How can antibodies to MHC arise?

A

→pregnancy

→blood transfusion or previous transplants

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17
Q

How do antibodies cause damage to transplanted tissue?

A

→Recognition of Fc region leading to -

→Complement activation

→Antibody dependent cellular cytotoxicity -(Fc Receptors on NK cells)

→Phagocytosis- (Fc Receptors on macrophages)

18
Q

Describe the process of hyperacute rejection

A

→Antibodies bind to endothelial cells

→complement fixation

→accumulation of innate immune cells

→Endothelial damage, platelets accumulate, thrombi develop

→

19
Q

What cells are activated in acute rejection?

A

→organ’s resident dendritic cells

20
Q

Why is there a Tcell response in acute rejection?

A

→MHC mismatch

21
Q

Describe the process of direct allorecognition of foreign MHC

A

→Inflammation results in activation of organ’s resident dendritic cells

→DC migrate to secondary lymphoid tissue where they encounter circulating effector T cells

→Macrophages and CTL increase inflammation and destroy transplant

22
Q

What happens in chronic rejection?

A

alloantibodies recruit inflammatory cells to blood vessel

→Blood vessel walls thickened, lumina narrowed – loss of blood supply

→Correlates with presence of antibodies to MHC-I

23
Q

What is the main cause of chronic rejection?

A

→indirect allorecognition of foreign MHC

24
Q

Describe the process of indirect allorecognition of foreign MHC

A

→Membrane fragments containing donor MHC are taken up by host DC

→Donor MHC is processed into peptides which are presented by host MHC

→T cell and antibody responses is generated to the peptide derived from processed donor MHC

25
Q

What type of transplant is haematopoietic stem cell transplant?

A

→autologous

26
Q

Where do

transplanted HSCs regenerate?

A

→bone marrow

27
Q

How are HSCs preserved?

A

→cyropreserved

28
Q

What is graft vs host disease?

A

→donor immune cells attacking the host

29
Q

What is one way of reducing GVHD?

A

→Removing T cells from transplant

→suppressing their function

30
Q

When are GVHD beneficial, and how?

A

→removing original leukemia
→Graft sees leukeamia is non-self
→may prevent disease relapse

31
Q

What are three classes of immunosuppressants for transplants?

A

→General immune inhibitors (e.g. corticosteroids)

→Cytotoxic – kill proliferating lymphocytes (e.g. mycophenolic acid, cyclophosphamide, methotrexate)

→Inhibit T-cell activation (cyclosporin, tacrolimus, rapamycin)

32
Q

What is cyclosporin?

A

→Blocks T cell proliferation and differentiation

33
Q

What is involved in combination immunosuppressive regimes?

A

→Steroids – e.g. prednisolone

→(2) Cytotoxic – e.g. mycophenolate motefil

→(3) Immunosuppressive specific for T cells – e.g. cyclosporin A, FK506

34
Q

Describe the induction stage of immunosuppression regime

A

→Antibody induction therapy

→Triple drug regimen

35
Q

What is involved in triple drug regimen?

A

→a calcineurin inhibitor, an antiproliferative agent, and corticosteroid

eg. Tacrolimus, mycophenolate mofetil, and prednisone is the most common regimen

36
Q

What is involved in the maintenance stage of immunosuppression regime?

A

→Triple drug regimen at lower doses- tapering off as time goes on

→No antibody regimen

37
Q

How is Tcell mediated rejection treated?

A

→ATG and steroids (eg, methylprednisolone 250-1000 mg per dose)

38
Q

How is Bcell mediated rejection treated?

A

→Intravenous immunoglobulin or anti-CD20 antibody and steroids.

39
Q

What are different types of immunosppressants?

A

→calcineurin inhibitors- inhibit IL-2 production

→antiproliferative- inhibit Tcell and Bcell proliferation

→corticosteroids

→mTOR inhibitors- blocks Tcell activation

→mAb antibodies- costimulation blockers

→IL-2 receptor antagonist

→antithymocyte globulins- inhibits and deplete Tcell

40
Q

What condition is cyclosporin liked with?

A

→nephrotoxicity

41
Q

Why is FMT used in immunosuppressed patients?

A

→promote effective anti-cancer immune responses

Defence (31 decks)

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