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CSP - Exam 4 > Grayson - Review > Flashcards

Grayson - Review Flashcards

1
Q

What inhibits NFAT?

A

Cyclosporin A. This prevents T cell activation by preventing IL-2 and CD25 production.

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2
Q 
Which of the following do not interfere directly with nucleotide synthesis?
A. Azothiaprine
B. Methotrexate
C. Prendozone
D. Cyclophosphamide
A

C. Prednosone, a synthetic corticosteroid drug that is particularly effective as an immunosuppressant drug. It is used to treat certain inflammatory diseases (such as moderate allergic reactions), some autoimmune diseases, and (at higher doses) some types of cancer, but it has significant adverse effects.

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3
Q

Predosone is a synthetic ___ drug that is particularly effective as an immunosuppressant drug.

A

Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant drug.

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4
Q

If I am a recipient T cell and I recognize donor HLA, what kind of recognition am I undergoing?

A

Direct recognition

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5
Q

What do we call the rejection of an organ that occurs within the first couple days to the first week or two? __
What if we see it within a day? __
What is it called when it takes a long time? ___

A

What do we call the rejection of an organ that occurs within the first couple days to the first week or two?
–>an acute rejection
What if we see it within a day?
–> a hyperacute rejection
What is it called when it takes a long time?
–> chronic rejection

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6
Q

What is a minor histo. complexus?

A

An intracellular protein.

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7
Q

How does poison ivy work? What type of HSR is this?

A

Pentadecacatechol binds to a self protein, making it a haptoprotein (altered self). This is presented to your T cell. This is a
Type IV HSR

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8
Q

What two diseases fall HEAVILY under type IV HSR?

A

Type 1 DM (CTL cells kill beta cells)

MS - the victims are the neurons, the perpetrator is the CD4 T cell –> loss of myelin sheath

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9
Q

What do Tregs express on their surface?

A

CD4 and CD25 and FOX3P

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10
Q

What happens if you don’t have FOX3P?

A

IPEX disease. This means you don’t get Treg (Remember, Treg cells have to be CD4+CD25+FOX3P) cells so you have an overactive immune system.

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11
Q

In the thymus, who protects us from getting self-reactive cells from other sites?

A

AIRE

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12
Q

What happens if you get a mutation in AIRE?

A

APECED –> you have wonky negative selection so you get self-reactive immune cells –> autoimmune syndromes.

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13
Q

What are some characteristics of a tumor?

A 
Uncontrolled growth
No signaling
Hypertrophy
Proliferate even if it "bumps up" against its neighbors
Undifferentiated
Elicits an immune response
Can initiate angiogenesis (VEGF)
Evades apoptosis
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14
Q

What is the role of PDL1?

A

Tumors express PDL1, an inhibitory receptor ligand. If you block the reaction between PDL1 on the tumor and PD1 on activated T cells, you get an increase in function of the activated T cell and in some cases, regression of tumor.

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15
Q

What key things do you need to do to the recipient before you give GVHD?

What do you have to lack in the recipient?

In the donor, what has to be in the bone marrow?

A

The patient needs to be immunosuppressed.

You have to lack functional T cells.

In the donor, functional T cells must be in the bone marrow.

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16
Q

If I take donor bone marrow and deplete it of T cells, will I increase or decrease GVHD in the recipient?
Why don’t you want to do this to a patient?

A

decrease.

You still need donor T cells to fight off potential viruses that were latent in the donor organ. Also, if it is a bone marrow transplant, the host still needs donor T cells to fight their cancer (GVT or GVL - graft versus tumor/graft versus leukemia). If you deplete the donor T cells, you won’t have T cells that can fight against the recipients tumors.

17
Q

In a human who is undergoing chemotherapy treatment, what kind of deficits do they have in their immune system?

A

Neutropenia, loss of T cells.

18
Q

In a person who has HIV, what cell are you lacking?

A

CD4 - susceptible to oportunistic infections.

19
Q

In a person who has HIV, what cell are you lacking?

A

CD4 - susceptible to opportunistic infections.

20
Q

Syngeneic graft is from an __

A

genetically similar organism (i.e. identical twin)

21
Q

Allogeneic graft is from an __

A

unrelated person but same species

22
Q

Xenogeneic graft is from __

A

unrelated species (pig heart valve, etc.)

23
Q 
4.	What type I hypersensitivity reaction does not require antibodies?
A.	Type III.
B.	Type IV.
C.	Type II.
D.	 Type I.
A

Type IV

24
Q 
1.	Joe Bob showed up to school one day irritated after a recent round of vaccinations. To cheer him up one of his friends, Peggy Sue, gave him a peanut butter cookie. His lips became swollen and he had trouble breathing. Upon visiting your clinic, his parents ask you to test him for peanut allergies. A small blood sample is withdrawn and you measure:
A.	Total IgG levels.
B.	Total IgE levels.
C.	Antigen-specific (peanut) IgG levels.
D.	Antigen-specific (peanut) IgE levels.
A

B. Total IgE levels.

25
Q

The disease IPEX is caused by mutations in:
A. CD25 that prevents T eff generation.
B. Bruton’s tyrosine kinase which blocks the development of T regs in the bone marrow.
C. TGF-beta mutations that block T reg generation.
D. Foxp3 that is required for T reg development and maintenance.

A

D. Foxp3 that is required for T reg development and maintenance.

26
Q
  1. T regs function by all of the following mechanisms except:
    A. Manipulation of metabolic microenvironment.
    B. Production of IL-10 and TGF beta.
    C. Killing of other lymphocytes.
    D. Induction of receptor editing in extrathymic CD4 cells.
A

D. Induction of receptor editing in extrathymic CD4 cells.

27
Q

Treg cells can manipulate the ____ microenvironment.

They also produce __ and ___. They are also involved in the killing of other ___.

A

A. metabolic microenvironment.
B. IL-10 and TGF beta.
C. other lymphocytes.

28
Q
  1. Which of the following is promising strategy to augment anti-tumor immune responses?
    A. Increasing the number of T regs.
    B. Blocking inhibitory receptor-ligand interactions.
    C. Depletion with anti-CD3e antibodies.
    D. Blocking TCR-HLA interactions with antibody THX1138.
A

B. Blocking inhibitory receptor-ligand interactions.

29
Q
  1. APECED is caused by mutations in:
    A. Fox 3p that prevent natural Treg development.
    B. Aire mutations that decrease negative selection.
    C. Aire mutations that increase positive selection.
    D. Aire mutations that control receptor editing in the bone marrow.
A

B. Aire mutations that decrease negative selection.

30
Q 
2.	The destruction of beta cells causes which autoimmune disease:
A.	Goodpasture Syndrome.
B.	Grave’s Disease.
C.	Jager’s-induced emesis.
D.	Type I diabetes.
A

D. Type I diabetes.

31
Q
  1. Which of the following is a diagnostic for SLE?
    A. anti-dsDNA antibodies.
    B. anti-IgG antibodies.
    C. anti-Acetylcholine receptor.
    D. anti-thyroid stimulating hormone receptor.
A

A. anti-dsDNA antibodies.

32
Q
  1. Epitope spreading refers to:
    A. Transfer of proteins between bacteria by plasmids.
    B. Transfer of proteins between viruses by reassortment.
    C. The activation of naive T cells by subsequent antigen exposure.
    D. The broadening of the specificity of self responses during autoimmunity.
A

D. The broadening of the specificity of self responses during autoimmunity.

33
Q
  1. Cancer cells must:
    A. Become resistant to apoptosis to cause malignant tumors.
    B. Become sensitive to contact inhibition to cause malignant tumors.
    C. Become more differentiated over time to cause malignant tumors.
    D. Become more dependent on external sources of growth factors to cause malignant tumors.
A
  1. Cancer cells must:

A. Become resistant to apoptosis to cause malignant tumors.

34
Q
  1. Syngeneic grafts:
    A. Differ in major and minor histocompatibility antigens.
    B. Possess the same major and minor histocompatibility antigens.
    C. Possess similar major but different minor histocompatibility antigens.
    D. Possess different major but similar minor histocompatibility antigens.
A

B. Possess the same major and minor histocompatibility antigens.

35
Q
  1. Direct allorecognition occurs when:
    A. Donor T cells recognize donor HLA on donor DCs.
    B. Donor T cells recognize host HLA on donor DCs.
    C. Host T cells recognize donor HLA on donor DCs.
    D. Host T cells recognize host HLA on donor DCs.
A

C. Host T cells recognize donor HLA on donor DCs.

36
Q 
3.	Which of the following deficiencies hinders adaptive immunity directly:
A.	Chronic granulomatous disease (CGD).
B.	C3 deficiency.
C.	X-linked agammaglobulinemia.
D.	IPEG.
A

C. X-linked agammaglobulinemia.

37
Q 
4.	Loss of which cell type precludes AIDS and death during HIV infection:
A. CD8+ T cells.
B. B cells.
C. NK cells.
D. CD4+ T cells.
A

D. CD4+ T cells.

38
Q 
5. FK506 and cyclosporine function by:
A. Directly blocking nucleotide synthesis.
B. Blocking NFAT nuclear translocation.
C. Inducing endonucleases in T cells.
D. Blocking inhibitory ligands.
A

B. Blocking NFAT nuclear translocation.

39
Q 
5.	Omalizumab is currently used to :
A.	Treat multiple sclerosis.
B.	Deplete B cells during cancer.
C.	Block inhibitory ligands.
D.	Treat chronic asthma.
A

D. Treat chronic asthma.

CSP - Exam 4 (22 decks)

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