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Immuno Exam Tres > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is immunological tolerance?

A

It’s specific unresponsiveness to an Ag (i.e. B + T cell trained not to recognized self thus don’t respond)

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2
Q

What is difference between central and peripheral tolerance?

A

Central tolerance is induced in IMMATURE self-reactive lymphocytes in PRIMARY LYMPHOID ORGANS
Peripheral tolerance is induced in MATURE self-reactive lymphocytes at PERIPHERAL sites

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3
Q

What are the fates of immature lymphocytes when they have self-specificity (central tolerance) (3 of them)

A
  1. Deleted
  2. Change BCR specificity (only B cells)
  3. Develop into Treg cells (T cells only)
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4
Q

What are the fates of mature lymphocytes when they have self-specificity (peripheral tolerance) (3 of them)

A
  1. Inactivated (anergy)
  2. Deleted (apoptosis)
  3. Suppressed by Treg cells
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5
Q

What receptor do Treg cells express high levels of? and what CDs do they have?

A

CTLA-4 which binds to CD80-86 on APCs –> turning them off.
They are CD4+ CD25+
CD25 –> is the IL-2 receptor

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6
Q

Is there a fundamental difference between the structure of auto-ags (self Ags) and non-self Ags

A

No there isn’t because all proteins composed of amino acids

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7
Q

What are the immune privileged sites? (7 of them).

A

Eye: cornea, anterior chamber, vitreous cavity and sub-retinal space, Brain (ventricles and striatum), pregnant uterus, ovary, testis, adrenal cortex, hair follices

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8
Q

What three words describe autoimmune diseases?

A
  1. Chronic
  2. Progressive
  3. Self-perpetuating
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9
Q

What is the cause of all autoimmune diseases?

A

Failure of B and T cell self-tolerance

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10
Q

Of the genes associated with autoimmunity which has the strongest association?

A

MHC genes

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11
Q

Most autoimmune diseases are associated with what class of HLA alleles? And what genes specifically?

A

Class II HLA alleles (HLA-DR and HLA-DQ)

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12
Q

What 4 mechanisms of microbial Ags can initiate an autoimmune response?

A
  1. Molecular mimicry
  2. Polyclonal (bystander) activation
  3. Epitope spreading
  4. Release of hidden/cryptic Ags
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13
Q

Are autoimmune diseases more common in men or women?

A

Women, for example, estrogen can exacerbate systemic lupus erythematosus

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14
Q

Is type-I diabetes a T or B cell mediated autoimmune disorder?

A

T cell-mediated

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15
Q

What is the difference between autografts, isografts, allografts, and xenografts?

A
  1. autografts –> graft coming from the same individual (like my ACL graft)
  2. Isograft –> graft exchange between different individuals that are genetically the same (i.e. twins)
  3. Allograft –> graft exchange between different people of same species
  4. Xenograft –> graft exchange between members of different species (pig to human)
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16
Q

What four variables determine transplant outcome?

A
  1. Condition of allograft
  2. Donor-host antigenic disparity (how different the Ags are of the host and donor if they’re similar then little response)
  3. Strength of host anti-donor response (is this the first time being presented or second time?)
  4. Immunosuppressive regimen
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17
Q

What is cold ischemia time?

A

Time organ is without blood circulation and is kept in cold to the time it is transplanted to the recipient and blood supply re-established

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18
Q

ABO blood groups are a barrier for what type of transplantation and for what types isn’t it a barrier?

A
  1. A barrier for solid organ transplants
  2. Not a barrier for:
    - corneal transplants
    - heart valve transplantation
    - bone and tendon grafts
    - stem cell transplantation
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19
Q

What are the Ags and Abs present for 1. A blood, 2. B blood, 3. AB blood, and 4. O blood

A
  1. Ag A, Ab B
  2. Ag B, Ab A
  3. Ag A and B, no Abs
  4. No Ags and Abs A and B
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20
Q

When testing for blood group, if there is agglutination does that indicate that it’s the correct blood type?

A

Yes as it means the Anti-Ag bound to the Ag confirming the blood type

21
Q

Difference between host vs graft disease and graft vs host disease

A

host v. graft is the host attacking the graft

graft v. host is the graft attacking the host

22
Q

There are 3 types of host vs graft reactions. What are the three and what is the onset for each? What are the mechanisms for each? Which are T cell mediated? Which is most common?

A
  1. Hyperaccute –> immediate
    - preformed Abs
    - blood type incompatibility
    - presents while still in surgery with thrombosis and occlusion
  2. Acute (most common) –> weeks to months (T cell mediated against foreign MHCs)
    - Results in inflammation and leukocyte infiltration of graft vessels
  3. Chronic –> months to years (T cell mediated due to foreign MHC “looking like” a self MHC)
    - results in thickening and fibrosis of graft vessels
23
Q

What is the main pathogenic mechanism for chronic graft rejection indirect or direct pathway?

A

Indirect pathway

24
Q

Does chronic rejection respond to immunosuppressive therapy?

A

no

25
Q

Is immune response seen against a graft more vigorous and strong that that seen against a pathogen?

A

yes

26
Q

There are two effector mechanisms for graft rejection what is the humoral one and what is the cellular one?

A

Humoral rejection is mediated by Th2 (IL-4, IL-5, and IL-10)
Cellular rejection is mediated by Th1 (IL-2, and IFN-y)

27
Q

What is the reaction in GVHD directed towards?

A

minor histocompatibility antigens (miHAs) of the recipient

28
Q

Differentiate between acute and chronic GVHD?

A
  1. Acute –> epithelial cell death in the skin, liver and GI

2. Chronic –> fibrosis and atrophy of affected organ

29
Q

Are patients on immunosuppressive drugs more prone to opportunistic infections and have raised risk of malignancy?

A

yes

30
Q

What is the mechanism of action of steroids/corticosteroids?

A
  1. Anti-inflammatory (by inhibiting the transcription of pro-inflammatory genes)
  2. Inhibit T-cell proliferation
  3. Induce lymphocyte apoptosis
    They are clinically used
31
Q

What is the mechanism of action of Cyclosporine A? what complex does it form? What is it used for?

A
  1. It inhibits the calcium-dependent pathway of T cell activation. Forms a calmodulin-calcineurin complex which inhibits the translocation of NFAT into nucleus thus inhibiting the transcription of IL-2, IL-3, IL-4, IL-5, IFN-y, TNF-a and GM-CSF
  2. Used for immunoprophylaxis in protocols for all types of organ transplants
32
Q

What is the mechanism of action of Anti-CD3 mAb (OKT 3)? For what kinds of solid organ transplants is it used?

A
  1. Inhibits T cell activation and depletion (CD3 is T cell signaling component so without it T cells can signal)
  2. ALL solid organ transplants, and used in prophylaxis (to prevent disease) and treatment of allograft rejection.
33
Q

What is the mechanism of action of Tacrolimus? when is it used?

A
  1. Inhibits IL-2 gene transcription. Same mechanism as Cyclosporin A where it blocks the Ca2+-dependent pathway of T cell activation and forms a complex (NOT same ONE) that inhibits translocation of NFAT inhibiting transcription of IL-2, IL-3, IL-4, IL-5, IFN-y, TNF-a and GM-CSF/
  2. Used for immunoprophylaxis in protocols for all types of organ transplants
34
Q

What is the mechanism of action of Anti-CD25 mAB?

A

Inhibits IL-2R signaling (IL-2 induces proliferation amongst other things so without the receptor T cells don’t proliferate)

35
Q

What is the mechanism of action of CTLA-4-Ig fusion protein?

A

Inhibition of the 2nd signal of T cell activation (inhibition of co-stimulation)

36
Q

What immunosuppressive drug is used for induction therapy (therapy administered at the time of organ transplantation) and is also used for the treatment of acute or steroid-resistant rejection?

A

Anti-CD3 mAb (OKT 3)

37
Q

What can calcineurin inhibitors lead to?

A

Kidney toxicity leading to graft loss

38
Q

What types of hypersensitivity reactions correspond to defenses against extracellular (antibody-mediated) pathogens?

A

Types I, II, and III

39
Q

What types of hypersensitivity reactions correspond to defenses against intracellular (cell-mediated) pathogens?

A

Type IV

40
Q

Immediate type I hypersensitivity is mediated by what?

A

Mediated by allergens and IgE Abs that activate mast cells and eosinophils to release inflammatory mediators

41
Q

Type II hypersensitivity is mediated by what? and in what manner?

A

Mediated by Abs that can bind to cell surface and tissue Ags and cause inflammation a complement-dependent manner

42
Q

Type III hypersensitivity is mediated by what? and in what manner?

A

Mediated by soluble Ag-Ab complexes in the circulation that are deposited in small vessels and capillaries and cause inflammation in the vessel wall (vasculitis) in a complement-dependent manner

43
Q

Type IV hypersensitivity is mediated by what? and in what manner?

A

Delayed reactions that are mediated by CD4+ Th1 and Th17 cells and CD8+ CTLs in a cytokine-dependent manner?

44
Q

What is atopy?

A

Genetic tendency to develop allergic disease.

45
Q

What are the mediators of type I hypersensitivity and their functions? (5 of them)

A
  1. Histamine (dilation of small vessels and increased vascular permeability)
  2. Proteases (causes tissue damage)
  3. Prostaglandins (vascular dilation)
  4. leukotrienes (smooth muscle contraction)
  5. Cytokines (induce local inflammation) (the late-phase reaction)
46
Q

Allergen testing is based on what type of hypersensitivity?

A

Local type I hypersensitivity

47
Q

What are the aims of allergen-SIT? (3)

A
  1. Induce peripheral T cell tolerance to allergens
  2. Increase threshold for mast cells and basophil activation by allergens
  3. Decrease IgE-mediated histamine release by mast cells
48
Q

What is the key mechanism of allergen-SIT?

A

Generation of induced regulatory FOXP3+ CD4+ CD25+ Treg Cells

Immuno Exam Tres (2 decks)

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