Module D Quiz Questions Flashcards

1
Q

Graves disease is caused by the production of thyroid-specific autoantibodies that bind to

the thyroid peroxidase and thyroglobulin.

the TSH receptor on the surface of thyroid epithelial cells.

the triiodothyronine receptor.

the glucagon receptor.

pancreatic  cells in the islets of Langerhans.

A

the TSH receptor on the surface of thyroid epithelial cells.

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2
Q

Which statement about peripheral tolerance is false?

Induction of anergy occurs in T cells and B cells that do not receive a costimulatory signal.

Cytotoxic T cell activity is necessary to destroy self-reactive cells in the peripheral tissues.

Regulatory T cells are involved in ensuring peripheral tolerance.

A costimulatory signal is necessary for B-cell activation.

Peripheral tolerance relies on the fact that an interaction with helper T cells is required for B-cell activation.

A

Cytotoxic T cell activity is necessary to destroy self-reactive cells in the peripheral tissues.

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3
Q

Which statement about tolerance to self-antigens is true?

Central tolerance occurs through negative selection in secondary lymphoid tissues, and peripheral tolerance occurs through induction of anergy as well as Treg cell activity.

Central and peripheral tolerance both occur in primary lymphoid tissues through negative selection.

Negative selection occurs in the peripheral tissues through the activity of cytotoxic T cells and the cytotoxins they produce.

Central tolerance occurs through negative selection in primary lymphoid tissues, and peripheral tolerance occurs through induction of anergy as well as Treg cell activity.

Tolerance is primarily determined via interactions with TH17 cells and the cytokines they secrete.

A

Central tolerance occurs through negative selection in primary lymphoid tissues, and peripheral tolerance occurs through induction of anergy as well as Treg cell activity.

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4
Q

Graves disease is caused by

autoantibodies to cardiac myosin, driving complement activation on the surface of heart muscle.

autoantibodies to pancreatic beta cell-specific proteins, including insulin, glutamate decarboxylase, and the phosphatase-related protein.

autoantibodies that bind to joint tissues, causing inflammatory responses.

autoantibodies that act as agonist antibodies when they bind to the TSH receptor.

autoantibodies that mediate antibody-dependent cell-mediated cytotoxicity of thyroid cells.

A

autoantibodies that act as agonist antibodies when they bind to the TSH receptor.

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5
Q

Hashimoto disease is caused by

autoantibodies that act as agonist antibodies when they bind to the TSH receptor.

autoantibodies to cardiac myosin, driving complement activation on the surface of heart muscle.

autoantibodies that mediate antibody-dependent cell-mediated cytotoxicity of thyroid cells.

autoantibodies to pancreatic beta cell-specific proteins, including insulin, glutamate decarboxylase, and the phosphatase-related protein.

autoantibodies that bind to joint tissues, causing inflammatory responses.

A

autoantibodies that mediate antibody-dependent cell-mediated cytotoxicity of thyroid cells.

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6
Q

Developing T cells and B cells that express receptors recognizing self-antigens are removed by

removal by cytotoxins produced by cytotoxic T cells.

NK cell deletion through negative selection.

induction of anergy.

negative stromal cell selection.

apoptosis through negative selection.

A

apoptosis through negative selection.

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7
Q

Eighty percent of autoimmune diseases occur in women. One hypothesis is that women are more susceptible to autoimmune diseases because they have two X chromosomes, while men have one. Why would having two X chromosomes make women more susceptible to autoimmune diseases?

Treg cells control X chromosome expression; failure of these cells to develop due to genetic mutations leads to an increased risk of autoimmune disease in women.

Hormonal regulation of the X chromosome in women’s cells fluctuates more, enhancing the risk of autoimmune disease.

The adaptive immune response reacts to the self antigens generated by random X inactivation in women’s cells.

The likelihood of autoimmunity is increased when immune system reacts to one of the two polymorphic antigens (one paternal, one maternal) from an X chromosome as a foreign molecule.

Men have paternal X chromosomes only, meaning they cannot inherit X-linked diseases through their mothers.

A

The likelihood of autoimmunity is increased when immune system reacts to one of the two polymorphic antigens (one paternal, one maternal) from an X chromosome as a foreign molecule.

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8
Q

An infectious agent that can trigger the development of rheumatic fever is

Streptococcus pyogenes.
Campylobacter jejuni.
Neisseria gonorrhoeae.
Staphylococcus aureus.
Escherichia coli.

A

Streptococcus pyogenes.

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9
Q

In the autoimmune disease _, production of antibodies that recognize antigens on Campylobacter jejuni and nervous system gangliosides can cause the targeting of nervous system cells for destruction.

Goodpasture syndrome
systemic lupus erythematosus
rheumatic fever
celiac disease
Guillain–Barré syndrome

A

Guillain–Barré syndrome

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10
Q

Which disease is caused by absence of the expression of AIRE?

Lupus erythematosus
Insulin-dependent diabetes mellitus
Autoimmune polyendocrine syndrome type 1
Graves disease
Rheumatoid arthritis

A

Autoimmune polyendocrine syndrome type 1

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11
Q

Corticosteroid treatment prevents lymphocytes from homing to a transplanted organ by

inhibiting interactions between cyclophilin and calcineurin.

inducing the engulfment of lymphocytes by professional phagocytes.

suppressing the release of Hsp90 from steroid hormone receptors.

increasing cellular levels of the NFκB inhibitor Iκb.

suppressing thymidine biosynthesis.

A

increasing cellular levels of the NFκB inhibitor Iκb.

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12
Q

The transplantation of a pig’s kidney into a human to treat end-stage renal disease is an example of

allograft.
autograft.
isograft.
histograft.
xenograft.

A

xenograft.

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13
Q

Which disorder can potentially be treated with bone marrow transplantation?

Sickle cell anemia
Kidney failure
Chronic obstructive pulmonary disease
Diabetes
Coronary artery disease

A

Sickle cell anemia

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14
Q

Alloreactions can be beneficial in the treatment of

severe-combined immunodeficiency.
leukemia.
sickle cell anemia.
diabetes.
Wiskott-Aldrich syndrome.

A

leukemia.

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15
Q

Hyperacute rejection mimics a _ reaction due to the involvement of antibody-mediated immune reactions.

graft-versus-host disease
type I hypersensitivity
type II hypersensitivity
type III hypersensitivity
type IV hypersensitivity

A

type II hypersensitivity

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16
Q

Which immunosuppressive drug is mismatched with its effect on the immune system?

Basiliximab – inhibition of IL-2 signaling
Prednisone – inhibition of inflammation
FK-506 – inhibition of T-cell activation
Belatacept – inhibition of costimulation
Rapamycin – inhibition of purine biosynthesis

A

Rapamycin – inhibition of purine biosynthesis

17
Q

Burkitt’s lymphoma results from an improper genetic recombination event involving the _ locus and the immunoglobulin heavy chain gene locus.

c-MYC
Cyclin D1
BCL-6
BCL-2
CCNDI

A

c-MYC

18
Q

Which type transplant utilizes tissue from a genetically identical donor?

Isograft
Xenograft
Autograft
Histograft
Allograft

A

Isograft

19
Q

Transplantation rejection is least likely to occur with which type of transplant?

Xenograft
Histograft
Allograft
Isograft
Autograft

A

Autograft

20
Q

Which of the following individuals is responsible for identifying the ABO blood types?

Karl Landsteiner
Jean-Baptiste Denys
Georges Mathé
John Kersey
Carl Bunger

A

Karl Landsteiner

21
Q

Once a proto-oncogene has become mutated and is no longer functional, it is referred to as a(n)

oncogene.
tumor-activating gene.
DNA repair gene.
viral oncogene
tumor-suppressor gene.

A

oncogene.

22
Q

Which of the following is a hallmark of cancer?

Susceptibility to apoptosis
Sensitivity to anti-growth signals
Insufficient growth signals
Limitless replicative potential
Impaired angiogenesis

A

Limitless replicative potential

23
Q

How do environmental mutagens increase the rate of mutations in cancer cells?

They cause changes to the cell cycle.

They increase the rate of DNA replication, resulting in more mutations.

They cause DNA damage, and mutations can occur during DNA repair.

They cause mistranslation of gene base pairs at random sites.

Cancer cells use mutagens as bases during DNA replication.

A

They cause DNA damage, and mutations can occur during DNA repair.

24
Q

Why are individuals with a mutation in one copy of the p53 tumor suppressor gene more likely to develop Li-Fraumeni syndrome?

The p53 protein forms a homodimer and mutation of one copy blocks the function of the other.

The p53 protein is a proto-oncogene and can cause cancer even if only one mutated copy is expressed.

Individuals with mutations in p53 are more susceptible to virus-induced tumors.

Only mutation of the second copy of the p53 gene is required for cancer development.

The p53 protein interacts with the BRCA1 gene to shut down cells with DNA damage.

A

Only mutation of the second copy of the p53 gene is required for cancer development.

25
Q

If a cancer cell has a mutation in TAP transporter protein what is the likely phenotype?

Lower levels of MHC class II on the cell surface

Lower levels of MHC class I on the cell surface

Decreased NK cell activity and increased T cell activity

Decreased NKG2D recognition of MIC by NK cells

Increased cell cycle progression

A

Lower levels of MHC class I on the cell surface

26
Q

Angiogenesis a critical step in the transition from a benign to malignant tumor because

connection to the circulatory system allows immune cells to invade the tumor.

there are more proto-oncogenes in tumors that have undergone angiogenesis.

cells not connected to the circulatory system have limited access to nutrients and oxygen.

angiogenesis prevents a tumor from metastasizing to new sites.

angiogenesis increases the DNA mutation rate, resulting in more aggressive tumors.

A

cells not connected to the circulatory system have limited access to nutrients and oxygen.

27
Q

Mutations that result in overexpression of normal proteins are called

tumor-specific antigens.
neoantigens.
viral antigens.
tumor-associated antigens.
mutagens.

A

tumor-associated antigens.

28
Q

How might persistent inflammation due to Helicobacter pylori infection result in gastric cancer?

Helicobacter pylori produces proto-oncogenes that result in cancer.

Persistent inflammation results in inactivation of the innate immune response and tumor escape from immune recognition.

Persistent inflammation activates the adaptive immune system, forcing cancer cells to become metastatic.

Production of reactive oxygen species by innate cells has the potential to modify bases and result in mutation during DNA repair.

Helicobacter pylori produces endotoxins that inhibit tumor suppressor genes.

A

Production of reactive oxygen species by innate cells has the potential to modify bases and result in mutation during DNA repair.

29
Q

Cancers associated with the immune system include

carcinoma.
hepatoma.
retinoblastoma.
sarcoma.
leukemia.

A

leukemia.

30
Q

What is myeloma?

Cancer caused by a virus
Cancer originating in the bone marrow
Cancer of muscle cells
B-cell tumors originating in the spleen
T-cell cancer originating in lymph tissues

A

B-cell tumors originating in the spleen