Fundamentals of Immunology Quiz
Fundamentals of Immunology: Death by Friendly Fire Quiz Answer | Week (1-3)

Coursera Fundamentals of Immunology Quiz: Death by Friendly Fire | Week (1-4)

Coursera Fundamentals of Immunology Quiz: Death by Friendly Fire | Week (1-4)

 
Fundamentals of Immunology: Death by Friendly Fire Quiz | Week (1-4)

 

 

Fundamentals of Immunology: Death by Friendly Fire

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Week- 1
Quiz 1

 
 
 
 
Question 1
1. Both __________ cells have αβ receptors.
  • NK; NKT
  • NKT; Treg
  • Tc; B
  • B; γδ
  • γδ; TH
  • TH; NK
 
Question 2
2. Both ___________ cells and fully adaptive, rearranging their receptor genes randomly and producing a vast number of different receptors.
 
  • NK; NKT
  • NKT; Treg
  • Tc; B
  • B; γδ
  • γδ; TH
  • TH; NK
 
Question 3
3. Macrophages and NK cells both have ________ receptors.
 
  • CD8 co-
  • CD3 co-
  • αβ TCR
  • γδ TCR
  • antibody (Fc)
  • inhibitory MHC I
 
 
Question 4
4. ______ have inhibitory MHC I receptors.
 
  • Only NK cells
  • Only Tc cells
  • Both NK and Tc cells
  • Neither NK nor Tc cells
 
 
Question 5
5. This picture shows an NK cell interacting with a viral-infected cell. The virus has blocked display of MHC I, although it cannot prevent the cell from showing signs of stress. The NK cell ______ attack because _______.
 
  • will; without MHC I inhibition, the stress ligand will prompt attack
  • will; the cell will activate ADCC in the NK cell
  • will not; there is no MHC I to activate attack
  • will not; there are no antibodies present to prompt ADCC
 
 
Question 6
6. This picture shows a CTL interacting with a healthy cell. The CTL ______ attack because _______.
 
  • will; it can bind to the peptides displayed the MHC I
  • will; the CTL has been activated by the TH cells
  • will not; the TCR and CD8 cannot recognize this type of MHC
  • will not; negative selection has removed any Tc cells that can recognize the antigen
 
 
Question 7
7. This picture shows a CTL cell infected with a virus capable of substituting its own fake MHC for the cell’s. The CTL ____ attack because _____.
 
  • will not; the TCR and CD8 cannot recognize this type of MHC
  • will not; negative selection has removed any Tc cells that can recognize the antigen
  • will; it can bind to the peptides displayed the MHC I
  • will; a CTL has been activated by the TH cells
 
 
Question 8
8. This drawing represents an NK cell from a mouse with a mutation that allows the MHC receptor to distinguish between native MHC and viral analogs. This cell _______ attack viral-infected cells displaying such analogs because these analogs _______.
 
  • will; display viral peptides
  • will; will not inhibit attack
  • will not; will inhibit the response
  • will not; deflect the apoptotic attack
 
 
Question 9
9. Scientists develop a number of mutant lines of mice with defective CTLs. Which of these, although disabled, nonetheless can still kill viral-infected cells?
 
  • cells with non-functioning perforin genes and functioning FAS-ligand genes
  • cells with non-functioning FAS-ligand genes and functioning perforin genes
  • cells with non-functioning versions of both perforin and FAS-ligand genes
  • A and B, but not C, will both be able to kill viral-infected cells.
  • All of these will be able to kill viral-infected cells.
 
 
Question 10
10. The conversion of LFA integrin on CTL cells from a high avidity conformation to a low avidity conformation triggers which of the following in a TC cell?
 
  • conjugate formation
  • fusion of vesicle with perforin and enzymes
  • initiation of apoptosis
  • signaling to the TH cells
  • dissociation from the target cell
 
 

Week- 2
Quiz 2

 
 

 

Question 1
1. PAMPs and DAMPs differ in that the ________.
  • PAMPs are derived directly from pathogens and the DAMPs from damaged self-tissue

     

  • PAMPs trigger the activation of IL-1, DAMPs do not.

     

  • PAMPs increased the inflammatory response, DAMPs lower it

     

  • DAMPs activate complement, PAMPs do not

     

  • PAMPs provide a better measure of the virulence and lethality of an infection

     

Question 2
2. Inflammatory chemokines bind to ________ receptors, which then activate ________.
  • seven-span; G proteins

     

  • seven-span; apoptosis

     

  • Ig; G proteins

     

  • Ig; integrins

     

  • tumor necrosis factor; apoptosis

     

  • tumor necrosis factor; integrins

     

Question 3
3. Based on its function, where would you be most likely to see HEV?
  • as part of the blood-brain barrier

     

  • facilitating oxygen exchange in the lungs

     

  • in vessels leading to lymph nodes, promoting extravasation of T cells

     

  • in the thymus, promoting exit of γδ cells

     

  • close to inflamed tissue, directing neutrophils and B cells to the infection

     

Question 4
4. The black pointer indicates an interaction that most directly leads to _________.
  • activation of NFAT in the neutrophil

     

  • stimulation of a toll-like receptor

     

  • shape changes in the neutrophil that cause it to insert between two endothelial cells

     

  • activation of G protein in the neutrophil

     

  • the neutrophil briefly adhering to the endothelium

     

Question 5
5. Which of the following CANNOT trigger assembly of the inflammasome
  • LPS

     

  • viral and bacterial DNA

     

  • alum

     

  • β-amyloid

     

  • UV light

     

  • Any of these things may trigger assembly and thus inflammation.

     

Question 6
6. In this picture of the inflammasome, the pointer labeled ___ indicates the site that recognized the danger signal, the arrow labeled _____ indicates the region most responsible for assembly of the overall heptamer and regions labeled _____ indicates the domain that clips the inactive IL-1 precursor, activating it.
  • I, II, III

     

  • I, III, II

     

  • II, I, III

     

  • II, III, I

     

  • III, I, II

     

  • III, II, I

     

 
Question 7
7. This compound is a __________ important in producing _________.
  • lipid; clotting and clot removal

     

  • lipid; pain and endothelial permeability

     

  • peptide; clotting and clot removal

     

  • peptide; pain and endothelial permeability

     

Question 8
8. Lipoxygenases are important in the production of ________ and cyclo-oxygenases are important in producing ____________.
  • leukotrienes; prostaglandins

     

  • leukotrienes; PAF

     

  • prostaglandins; leukotrienes

     

  • prostaglandins, PAF

     

  • PAF; prostaglandins

     

  • PAF; leukotrienes

     

 
Question 9
9. The hydrolysis shown here by the yellow line is most directly triggered by the action of _______.
  • Hageman’s factor

     

  • thrombin

     

  • kallikrein

     

  • cyclo-oxygenases

     

  • GTP produce by G proteins

     

Question 10
10. Pus formation largely results from the accumulation of the remains of dead and dying ________.
  • neutrophils

     

  • macrophages

     

  • epithelial cells

     

  • sentinel dendritic cells

     

  • red blood cells and platelets

     

 

Week- 3
Quiz 3


 
 
 

 

 
Question 1
1. This molecule is activated when it _______, after which it promotes immune _______.
 
  • is hydrolyzed by an inflammasome; tolerance

     

  • is hydrolyzed by an inflammasome; inflammation

     

  • releases an inhibitor; tolerance

     

  • releases an inhibitor; inflammation

     

 
 
Question 2
2. The rel domains of the NFκB N-terminal domain can bind to _______
 
  • the enhancer region of pro-inflammatory genes

     

  • IκB (the inhibitor)

     

  • spectrin

     

  • A and B

     

  • A and C

     

  • B and C

     

 
 
Question 3
3. Which of the following is NOT likely to trigger a danger signal to the immune system?
 
  • environmental toxins and irritants

     

  • normal biomolecular components located where they shouldn’t be

     

  • molecules normally produced only by bacteria

     

  • breakdown products of hyaluronin and beta amyloid precursor

     

  • protein hormones secreted by the pancreas

     

 
 
Question 4
4. A series of events leads to the assembly of the inflammasome, some of which are listed below.
 
I. NLR bind danger signals.
 
II. Card domains of ASC and caspase bind.
 
III. Card domains of NLR and ASC bind.
 
IV. Heptamer assembles.
 
  • I, II, III, IV

     

  • IV, III, II, I

     

  • I, III, II, IV

     

  • I, III, IV, II

     

  • III, I, IV, III

     

 
 
Question 5
5. Generally B cells become anergic based on their interactions, or lack thereof, with T cells. Which of the following does not describe a situation where a B cell would leave the bone marrow and then essentially shut down.
  • The B cell find a TH to synapse with and then the TH cell releases IL-2.

     

  • A Treg cell synapses with it, and instructs the B cell to become anergic.

     

  • The B cell cannot find a TH to simulate it because all the TH cells that can bind the antigen have been deleted in the thymus.

     

  • The B cell cannot find a TH to simulate it because all the TH cells that can bind the antigen have encountered sentinel dendritic cells that did not produce B7.

     

 
 
Question 6
6. Scientists engineer a mouse by inserting the gene for aequorin, a protein that glows green when exposed to Ca2+, into their genomes. Mouse 1 produces aequorin in the plasma, but not the bone marrow. Mouse 2 produces aequorin on the surface of most of its cells. When the scientists look for B cells that react to aequorin, they find_______.
 
  • reactive cells in the bone marrow of both mice, and reactive cells in the plasma of mouse 1, but not 2

     

  • reactive cells in the bone marrow of both mice, and reactive cells in the plasma of mouse 2, but not 1

     

  • no reactive cells in the plasma of either mouse, but reactive cells in the bone marrow of mouse 1

     

  • no reactive cells in the plasma of either mouse, but reactive cells in the bone marrow of mouse 2

     

 
 
Question 7
7. The high concentration of CTLA 4 on the surfaces of Treg cells functions to allows the cell to ________.
 
  • attach to presenting dendritic cells

     

  • extravasate into secondary lymphoid organs

     

  • recognize self antigen

     

  • activate and undergo clonal expansion before other CD4+ cells can

     

  • deplete the B7 in its vicinity

     

 
 
Question 8
8. The hexokinase molecule binds ___________ as a substrate at the active site and at an allosteric site inhibiting the enzyme. The inhibitory (allosteric) site has a relatively _________ binding affinity than does the active site.
 
  • the same compound; higher

     

  • the same compound; lower

     

  • different compounds; higher

     

  • different compounds; lower

     

 
 
Question 9
9. Mutations that block the signal indicated by the blue arrow will result in autoimmunity resulting from a failure of _________.
 
  • Treg cell production

     

  • negative selection due to T cell exposure to too few self-antigens

     

  • positive selection due to inability to display either CD4 or CD8

     

  • negative selection due to cells escaping instructions to undergo apoptosis

     

  • T cells synthesis of the cell surface molecules necessary to extravasate into the lymph nodes

     

 
 
Question 10
10. Fezf2 functions by ________.
  • loosening the binding between histones and DNA

     

  • inducing the differentiation of Treg cells

     

  • binding to the enhancer regions of a wide variety of genes

     

  • triggering an internal pathway leading to apoptosis

     

  • inhibiting immune upregulation in the absence of danger signals

     

Week- 4
Quiz 4


 


Question 1
1. Which autoimmune disease results in the production of the widest variety antibodies and TC cells to different antigens?
1 point
  • Ulcerative Colitis
  • Hashimoto’s Thyroiditis
  • MS (Multiple Sclerosis)
  • Myasthenia Gravis
  • SLE (Lupus)

Question 2

2. Which of the following is classified as a systemic autoimmune disease, as opposed to one that is organ or tissue specific?

 

  • Crohn’s Disease
  • Rheumatoid Arthritis
  • Hasimoto’s Thyroiditis
  • Type I Diabetes
  • Psoriasis

Question 3

Which one of these autoimmune diseases seems to be triggered more by excessive innate signals than by adaptive signals gone wrong?

 

  • Psoriasis
  • Myasthenia Gravis
  • SLE (Lupus)
  • MS (Multiple Sclerosis)
  • Hashimoto’s Thryoiditis

Question 4

4. Which of the following autoimmune diseases results in overstimulation of either an endocrine or nerve cell?

 

  • Type I Diabetes
  • Hashimoto’s Thyroiditis
  • Graves’ Disease
  • Psoriasis
  • Myasthenia Gravis

Question 5

5. Which of the following autoimmune diseases results primarily from the actions of antibody, with cell destruction not a necessary part of the symptoms?

 

  • Type I Diabetes
  • Ulcerative Colitis
  • Psoriasis
  • Myasthenia Gravis
  • MS (multiple sclerosis)

Question 6

6. Which of the following autoimmune diseases disrupts a person’s ability to move because the nerve axons cannot effectively transmit the stimulating signal?

 

  • Crohn’s Disease
  • Psoriasis
  • MS (Multiple Sclerosis)
  • Myasthenia Gravis
  • Graves’ Disease

Question 7

7. Which of the following diseases directs its attack on cells lining the gut?

 

  • Hashimoto’s Thyroiditis
  • Crohn’s Disease
  • Rheumatoid Arthritis
  • Psoriasis
  • MS (Multiple Sclerosis)

Question 8

8. Which of the following autoimmune diseases results from destroying cells that need to supply one of the body’s hormones?

 

  • Psoriasis
  • Graves’ Disease
  • Myasthenia Gravis
  • Lupus (SLE)
  • Hashimoto’s Thyroiditis

Question 9

9. Vitamin D decreases the ______.

 

  • Number of circulating Treg cells
  • Release of pro-inflammatory cytokines
  • Effectiveness of negative selection in the thymus
  • Production of erythrocytes in the bone marrow
  •  

  •  

  •  

  •  

 

Question 10

10. __________ can help treat autoimmune disease by _________.

 

  • Anti-hygiene therapies; switching the body to TH2 response.
  • Plasmapheresis; removing reactive T cells
  • CTLA 4 antibodies; supply the B7 co-stimulus
  • IL-2; activating Treg cells
  • Statins; increasing inflammatory cytokines
 

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