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Allergy/Immunology Board Review FIT Corner Questions from Middleton's > Immune Mechanisms 2018-2020 > Flashcards

Immune Mechanisms 2018-2020 Flashcards

1
Q 
1. Which of the following selectins is located on leukocytes?
A. E-selectin
B. L-selectin
C. P-selectin
D. Z-selectin
A
  1. B, L-selectin, p. 41-42.
    L-selectin is located on leukocytes. P-selectin and E-selectin are located on endothelial cells.
    Z-selectin is a fictitious selectin.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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2
Q 
2. Which of the following is a correct pairing of the chemokine with its original name?
A. CCL5:IL-8
B. CCL11:Eotaxin
C. CL21:TARC
D. XCL1:MIF-2a
A
  1. B, CCL11:Eotaxin, p. 44.

CCL21 is SLC. CCL17 is TARC. It is important to know that CCL11 is eotaxin. CCL5 is RANTES.
XCL1 is lymphotactin.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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3
Q
  1. What is the defect in type 1 leukocyte adhesion deficiency?
    A. Error in encoding ICAM-1, ICAM-2, and ICAM-3
    B. Inability to encode the beta subunit of LFA-1 and MAC-1
    C. Lack of the Golgi GDP-fructose transporter needed to express the carbohydrate ligand.
    D. Mutation in the signaling pathways linking chemokine receptors to integrin activation
A
  1. B, Inability to encode the beta subunit of LFA-1 and MAC-1, p. 45-46.
    Type 1 leukocyte adhesion disorder is due to an inability to encode the beta subunit of LFA-1 and MAC-1. It is an autosomal recessive inherited deficiency in the CD18 gene.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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4
Q
  1. What is the defect in type 2 leukocyte adhesion deficiency?
    A. Error in encoding ICAM-1, ICAM-2, and ICAM-3
    B. Inability to encode the beta subunit of LFA-1 and MAC-1
    C. Lack of the Golgi GDP-fructose transporter needed to express the carbohydrate ligands for E-selectin and P-selectin
    D. Mutation in the signaling pathways linking chemokine receptors to integrin activation
A
  1. C, Lack of the Golgi GDP-fructose transporter needed to express the carbohydrate ligands for E-selectin and P-selectin, p. 46.

Type 2 leukocyte adhesion deficiency is due to the lack of the Golgi GDP-fructose transporter needed to express the carbohydrate ligands for E-selectin and P-selectin.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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5
Q
  1. How does the sphingosine 1-phosphate (S1P) gradient drive T-cells from the blood into the lymph nodes?
    A. High levels of S1P in the blood cause internalization of S1PR1, thus allowing naïve T-cells in the lymph node to remain until externalization of S1PR1 increases due to the gradient
    B. levels of S1P in the lymph nodes compared to the blood drive naïve T-cells into the lymph node, where the naïve T-cells downregulate S1PR1 to remain in the lymph node
    C. High levels of S1P in the lymph nodes compared to the blood drive naïve T-cells into the lymph node, where the naive T-cells upregulate S1PR1 to remain in the lymph node
    D. S1P binds to S1PR1 in blood causing a cascade that leads naïve T-cells to migrate into the lymph node
A
  1. A, High levels of S1P in the blood cause internalization of S1PR1, thus allowing naïve Tcells in the lymph node to remain until externalization of S1PR1 increases due to the gradient, p. 51.
    S1PR1 stimulates migration of cells towards a gradient of S1P. Circulating naïve T cells have very little surface S1PR1 because the high blood concentration of S1P causes internalization of the receptor. After a naïve T cell enters a lymph node, where S1P concentrations are low,
    S1PR1 reappears on the cell surface over a period of several days.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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6
Q 
6. Which protein helps activated naïve T-cells remain in the lymph node?
A. Albumin
B. CD31
C. CD69
D. Ficolin
A
  1. C, CD69, p. 52.
    CD69 is a protein that binds S1PR1 and reduces its cell surface expression. This prevents the naïve T cell from migrating from the lymph node to the blood, where the concentration of S1P is higher.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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7
Q 
7. Which of the following chemokine receptors is important for B cells to migrate into the white pulp of the spleen?
A. CXCR4
B. CXCR5
C. CCXR7
D. CXCR8
A
  1. B, CXCR5, p. 53.
    CXCR5 promotes the movement of B cells into the white pulp in response to CXCL13.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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8
Q 
8. What do bone marrow-homing IgG-secreting plasma cells express?
A. CXCR4 and CCR9
B. LFA-1 and VLA-4
C. VLA-4 and CXR4
D. VLA-4 and CCR9
A
  1. C, VLA-4 and CXCR4, p. 55.
    VLA-4 and CXCR4, which bind respectively to VCAM-1 and CXCL12, expressed on bone marrow sinusoidal endothelial cells.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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9
Q 
9. Which chemokine receptor plays a critical role in dendritic cell migration into the lymph nodes and is expressed at high levels on naïve T-cells to promote their interaction?
A. CCR5
B. CCR7
C. CXCR5
D. CXCR7
A
  1. B, CCR7, p. 49.
    CCR7 is expressed at high levels on naïve T cells. CCL19 and CCL21 interaction with CCR7 ensures that naïve T cells increase integrin avidity and can adhere firmly to HEVs. Shared expression of CCR7 between naïve T cells and dendritic cells maximizes the chances of the two cells interacting.

Chapter 3: Leukocyte Circulation and Migration into Tissues
Cellular and Molecular Immunology, 9th edition

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10
Q 
1. Which of the following Toll Like Receptors (TLRs) is located on the cell membrane?
A. TLR2
B. TLR3
C. TLR7
D. TLR8
A
  1. A, TLR2, p. 63.
    Toll Like Receptors are a family of pattern recognition receptors expressed on many cell types that recognize a wide variety of microbes. TLR2 is located on the cell membrane and
    recognizes bacterial peptidoglycan and lipopeptides. The cellular membrane TLRs are 1, 2, 4, 5, 6.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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11
Q 
2. Genetic deficiency in UNC-93B results in susceptibility to:
A. candidal infections.
B. HSV encephalitis.
C. staphylococcal infections.
D. streptococcal pneumonia.
A
  1. B, HSV encephalitis, p. 64.
    UNC-93B is a protein on the endoplasmic reticulum required for endosomal localization and proper function of TLR 3, 7, 8 and 9. Endosomal TLRs recognize dsRNA (TLR3), ssRNA (TLR7)
    and unmethylated CpG motifs in DNA (TLR9). The endosomal location of ssRNA and dsRNA reflects microbial origin. The mutation in UNC-93B reflects the importance of the endosomal
    location of TLRs for innate defense against viruses.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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12
Q 
3. What is used to treat cryopyrin-associated periodic syndrome (CAPS)?
A. IFNγ
B. IL-1R antagonist
C. IL-5 antagonist
D. Rituximab
A
  1. B, IL-1R antagonist, p. 69-71.
    Muckle-Wells, NOMID, FCAS are due to a mutation in NLRP3 (aka cryopyrin), resulting in cryopyrin-associated periodic syndrome (CAPS). IL-1 and IL-1R antagonists, canakinumab and anakinra respectively, can be used to treat these disorders as IL-1 is generated from pro-IL-1β in the NLRP3 inflammasome.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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13
Q 
4. Which cytokine is necessary for Th1 differentiation?
A. IL-10
B. IL-12
C. IL-15
D. IL-23
A
  1. B, IL-12, p. 83-86.
    IL-12 is secreted by dendritic cells and macrophages. It is produced in response to TLR signaling from bacterial LPS or lipoteichoic acid and virus infections.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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14
Q
  1. Type 1 interferons (IFN-α and IFN-β) act through which mechanism?
    A. Promote naïve T cell differentiation to Th17 cells
    B. Sequestration of lymphocytes in lymph nodes
    C. Stimulating adaptive immune response via two-signal hypothesis
    D. Upregulating class II MHC molecules
A
  1. B, Sequestration of lymphocytes in lymph nodes, p. 90-92.
    Type 1 interferons protect against viral infections by sequestering lymphocytes in lymph nodes, increasing cytotoxicity of NK cells, upregulating class I MHC molecules, increasing the
    probability that virally infected cells will be killed by CD8 cells, and promoting differentiation of naïve T cells to Th1 cells. The two-signal hypothesis states that lymphocytes require activation from both an antigen as well as additional stimuli such as cytokines. This prevents
    the adaptive immune cells from attacking normal cells and tissues.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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15
Q
  1. ILC2 cells:
    A. are activated by IL-7 and IL-15.
    B. are important for defense against helminthic parasites.
    C. are important for defense against extracellular fungi.
    D. resemble Th1 cells.
A
  1. C, are important for defense against extracellular fungi, p. 74-75.

ILC2 cells resemble Th2 cells. Their development is dependent on IL-7 (ILC1 cells require IL-7 and IL-15). ILC2 are important for defense against helminthic parasites and may contribute to allergic diseases. ILC3 cells participate in defense against extracellular fungi.

Chapter 4: Innate Immunity
Cellular and Molecular Immunology, 9th edition

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16
Q 
1. Which of the following is true about IgG?
A. Binds to the neonatal FcRn receptor
B. Forms a pentamer
C. Has a half-life of 5 days
D. Has 2 subtypes
A
  1. A, Binds to the neonatal FcRn receptor, pg 38-41.

IgM is secreted as a pentamer of five IgM monomers linked together by disulfide bonds with the J-chain. IgM has a half-life of five days. There are two subclasses of IgA, IgA1 and IgA2, and can exist as monomers or dimers.

Endothelial cells and monocytes express the neonatal Fc receptor for IgG (FcRn) that internalizes serum IgG and can the recycle IgG molecules back into the circulation.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

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17
Q 
2. What is the strength of the binding between a single combining site of an antibody and epitope of an antigen called?
A. Avidity
B. Affinity
C. Affinity maturation
D. Diversity
A
  1. B, Affinity, 31-36.
    Antibodies and antigens are multivalent – with specific antigens possessing more than one binding site.

Avidity is a semiquantitative term used to describe the overall binding of
antibodies to antigen at all antigen binding sites.

Affinity refers to the strength of a single antigen-antibody interaction. Antibodies with fewer binding sites may have higher affinity and lower avidity, while those with greater binding sites may have lower affinity and higher avidity. Affinity maturation refers to the somatic hypermutation process largely seen in IgG antibodies, but also found in IgA and IgE species. V(D)J light and heavy chain gene rearrangements contribute to the generation of immunoglobulin diversity.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

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18
Q
  1. Which of the following is true about the VL and VH domains of antibodies?
    A. Located at the carboxy terminus
    B. Located in the Fab portion of the antibody
    C. Located in the Fc portion of the antibody
    D. Do not participate in antigen binding
A
  1. B, Located in the Fab portion of the antibody, pg 99.
    VL and VH domains of an antibody are located in the Fab portion of the antibody. They are located at the amino- terminus of the antibody. VL and VH domains of an antibody participate in antigen recognition.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

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19
Q
  1. Which of the following is true about Papain digestion of an antibody?
    A. Generates a single bivalent antigen-binding fragment, F(ab’)2
    B. Cleaves between the VL and CL region of the antibody
    C. Cleaves between the VH and the CH1 region of the antibody
    D. Allows the separation of 2 Fab fragments from the Fc fragment
A
  1. D, Allows the separation of 2 Fab fragments from the Fc fragment, pg 101.
    If rabbit IgG is treated with the enzyme papain, the enzyme acts on the hinge region and cleaves the IgG into three separate pieces. Two of the pieces are identical and consist of the light chain VL and CL associated with the VH and CH1 fragment of the heavy chain. The third piece is composed of two identical disulfide linked peptides each containing CH2 and CH3.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

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20
Q 
5. Immature B cells produce:
A. Membrane IgD.
B. Membrane IgM.
C. Membrane IgM and IgD.
D. No immunoglobulins.
A
  1. B, Membrane IgM, pg 108-109.
    Immature B cells produce membrane IgM. Mature B cells produce membrane IgM and IgD.
    Antibody secreting cells produce high rates of IgM, IgG, IgA, or IgE secretion.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

21
Q
  1. Membrane forms of Ig heavy chains:
    A. contain transmembrane regions made up of hydrophilic amino acid residues.
    B. contain transmembrane regions made up of hydrophobic amino acid residues.
    C. ends in C terminal tail pieces.
    D. have similar cytoplasmic domains that are identical between isotypes.
A
  1. A, Contains transmembrane regions made up of hydrophilic amino acid residues, pg 105.
    The membrane forms of the Ig heavy chains have hydrophilic amino acid residues, but not the secreted forms contain transmembrane regions made up of hydrophobic amino acid residues. The cytoplasmic domains differ between the different isotypes.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

22
Q 
7. Which of the following is true about antibodies?
A. IgA has 4 subtypes
B. IgE has a half-life of 2 days
C. IgG is a pentamer
D. IgM is a monomer
A
  1. B, IgE has a half-life of 2 days, pg 104.
    The flexibility of the antibody is mainly due to the hinge regions located between the CH1 and CH2 domains, which permit independent movement of antigen binding sites relative to the rest of the molecule.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

23
Q
  1. The hinge region:
    A. allows for rigidity in the antibody structure.
    B. allows for rotation between the CH2 and CH3 domains.
    C. is located between the CH1 and CH2 domains.
    D. is located between the CH2 and CH3 domains.
A
  1. C, Is located between the CH1 and CH2 domains, pg 104.
    The flexibility of the antibody is mainly due to the hinge regions located between the CH1 and CH2 domains, which permit independent movement of antigen binding sites relative to the rest
    of the molecule.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

24
Q
  1. Tumor necrosis factor (TNF) is associated with which disease states?
    A. Allergy-related asthma
    B. Cardiovascular disease
    C. Multiple sclerosis
    D. Rheumatoid arthritis, Crohn’s disease, psoriasis
A
  1. D, Rheumatoid arthritis, Crohn’s disease, psoriasis, pg 108.
    Immature B cells produce membrane IgM. Mature B cells produce membrane IgM and IgD.
    Antibody secreting cells produce high rates of IgM, IgG, IgA, or IgE secretion.

Chapter 5: Antibodies and Antigens
Cellular and Molecular Immunology, 9th edition

25
Q 
1. Which chromosome contains the MCH locus?
A. Chromosome 2
B. Chromosome 4
C. Chromosome 6
D. Chromosome 8
A 
1. C, Chromosome 6, pg 125.
There are three class I MHC genes called HLA-A, HLA-B, HLA-C and three class II HLA gene loci called HLA-DP, HLA-DQ, and HLA-DR.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

26
Q 
2. Which of the following is found in the MHC III locus?
A. HLA-A
B. HLA-DP
C. HLA-DR
D. TNF-α
A
  1. D, TNF-α.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

27
Q
  1. Which of the following statements about MHC is true?
    A. Each MHC can only bind only one unique peptide with a unique and specific amino acid sequence
    B. MHC complexes only bind foreign (non-self) peptides
    C. MHC I can bind a longer peptide than MHCII
    D. Very small numbers of peptide-MHC complexes are capable of activating specific T lymphocytes
A
  1. D, Very small numbers of peptide-MHC complexes are capable of activating specific T lymphocytes, pg 130-132.
    Very small numbers of peptide-MHC complexes are capable of activating specific T lymphocytes. Because APCs continuously present peptides derived from all proteins, only a very small fraction of surface peptide-MHC complexes will activate a specific T cell response.
    Unlike MHCI, the MHC II peptide binding groove is open on each end, which allows a longer peptide to bind (up to 10-30 amino acids). Each MHC molecule (I or II) can only bind one peptide at a time but can bind many different peptides. MHC molecules from an individual can bind and display foreign or self-antigens.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

28
Q 
4. Mutations in which of the following genes results in X-linked hyper IgM syndrome?
A. AID
B. CD40
C. CD40L
D. UNG
A
  1. C, CD40L.
    AID, CD40 and UNG mutations are associated with hyper IgM syndromes type 2, 3 and 5, respectively. These are all autosomal recessive.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

29
Q
  1. Which of the following is true about class I MHC pathway?
    A. Digestion of protein occurs in endosomes/lysosomes
    B. Digestion of protein occurs via proteasome
    C. Endocytosis of extracellular protein is required
    D. Protein is expressed on cell surface to CD4+ T cells
A
  1. B, Digestion of protein in proteasome.
    Class I MHC molecules are typically intracellular molecules and are presented on cell surface to CD8+ T cells.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

30
Q
  1. What effect does successful presentation of an antigen on MHC I to T cells have on surrounding cells and tissues?
    A. Activates surrounding macrophages to kill microbes
    B. Stimulates B cells to secrete antibodies
    C. Stimulates CD8+ T cells to kill antigen-expressing target cell
    D. Triggers release of cytokines
A 
6. C, Stimulates CD8+ T cells to kill antigen-expressing target cell.
The other effects are class II MHC presentation.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

31
Q 
7. Where does affinity maturation occur in the lymph node?
A. Germinal center
B. Marginal zone
C. Parafollicular area
D. Subcapsular sinus
A
  1. A, Germinal center.
    Affinity maturation occurs in the germinal center of the lymph node.

Chapter 6: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

32
Q 
1. Which type of cellular receptor is an integral membrane protein with intrinsic catalytic enzyme domain(s) in the cytoplasmic tail?
A. G-protein coupled receptor
B. Non-receptor tyrosine kinase
C. Nuclear receptor
D. Receptor tyrosine kinase
A
  1. D, Receptor tyrosine kinase, pg 147.
    Receptor tyrosine kinases are integral membrane proteins that activate an intrinsic tyrosine kinase domain (or domains) located in the cytoplasmic tails of the receptors when they are
    cross-linked by multivalent extracellular ligands. Non-receptor tyrosine kinases do not have intrinsic catalytic activity in their cytoplasmic tails. Nuclear receptors are intracellular, and G
    protein-coupled receptors are associated with GTP-binding proteins which then interact with enzymes downstream.

Chapter 7: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

33
Q 
2. A 45-year-old, poorly controlled diabetic patient develops progressive renal failure and requires a renal transplant. He is placed on tacrolimus as part of his immunosuppressive regimen. Tacrolimus complexes with FKBP inhibits what molecule, thus blocking NFAT translocation into the nucleus?
A. Calcineurin
B. Cyclophilin
C. FK506
D. NF-kB
A
  1. A, Calcineurin, pg 163.
    Tacrolimus binds to a protein called FK506-binding protein (FKBP). This complex inhibits calcineurin.

Cyclosporine binds to cyclophilin, also inhibiting calcineurin. Inhibition of calcineurin blocks translocation of NFAT into the nucleus. FK506 is another name for tacrolimus, and NF-kB is not directly affected by either tacrolimus or cyclosporine.

Chapter 7: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

34
Q 
3. Type II cytokine receptors (interferon receptor family) utilize which signaling pathway?
A. JAK-STAT
B. PKC-β
C. NF-κB
D. Ras-MAP kinase
A
  1. A, JAK-STAT, pg 171.
    All of the type II receptors engage JAK-STAT signaling pathways. Type I cytokine receptors also use the JAK-STAT pathway. The other listed proteins are involved in signaling, but type II
    cytokine receptors do not use these pathways.

Chapter 7: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

35
Q 
4. Which of the following is a ligand for the IL-1 receptor family?
A. IL-2
B. IL-10
C. IL-18
D. IFN-γ
A
  1. C, IL-18, pg 172.
    IL-18 and IL-1 are both ligands of the IL-1 receptor family, and both of these cytokines are involved in activity of the inflammasome. The receptors of this family share a conserved cytosolic sequence called the Toll/IL-1 receptor (TIR) domain and engage similar signal
    transduction pathways.

IL-10 and IFN-γ are ligands of type II cytokine receptors, and IL-2 engages a type I cytokine receptor.

Chapter 7: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

36
Q 
5. Gain-of-function mutations in which of the following cause myelodysplastic syndrome?
A. JAK2
B. JAK3
C. STAT1
D. STAT3
A
  1. A, JAK2, pg 175.
    Gain-of-function mutations in JAK2 can cause of myelodysplastic syndrome with varying phenotypes of aplastic anemia and polycythemia vera.

Type I cytokine receptors of the IL-6 family use JAK2 to activate STAT3, but STAT3 can also be activated by several other cytokines. Mutations affecting JAK3 can lead to a form of SCID similar to common γ chain deficiency. Negative mutations in STAT3 can lead to problems with Th17 responses leading to an immunodeficiency disease while activating mutations seen in large granular lymphocytic leukemias.

Chapter 7: Immune Receptors and Signal Transduction
Cellular and Molecular Immunology, 9th edition

37
Q
  1. What is one mechanism used by humoral immunity to protect against microbes?
    A. Antibodies block the binding of microbes to their receptors
    B. Antibodies phagocytose microbes and microbial toxins
    C. Antibodies release mediators to cause local inflammation
    D. Antibodies release mediators to lyse microbes
A
  1. A, Antibodies block the binding of microbes to their receptors, pg 276-277.
    Antibodies block the binding of microbes and microbial toxins to cellular receptors, thus neutralizing or inhibiting the infectivity of microbes and minimizing the injurious effects of microbial toxins. Antibodies neutralize microbes and toxins, opsonize them for phagocytosis, sensitize them for antibody-dependent cellular-cytotoxicity, and activate the complement system. Different antibody types mediate various effector functions.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

38
Q
  1. Which of the following is an accurate description of one of the effector mechanisms of adaptive immunity?
    A. Antibodies coat microbial surfaces to promote phagocytosis
    B. Complement proteins actively phagocytose microbes
    C. Mononuclear phagocytes and neutrophils directly bind and ingest microbes
    D. Neutrophils bind microbial surface receptors to cause self-destruction
A
  1. A, Antibodies coat microbial surfaces to promote phagocytosis, pg 275.
    IgG antibodies coat (opsonize) microbes and promote their phagocytosis by binding to Fc receptors on phagocytes. Choice A describes a function of the innate immune system in protection against microbes.

Neutrophils can ingest microbes, but do not cause microbial
self-destruction. Complement can play a role in active immunity as C3b coats microbes and leads to phagocytosis but complement proteins themselves do not phagocytose microbes.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

39
Q
  1. What is one mechanism for the therapeutic benefit of IVIG therapy in autoimmune disorders?
    A. Antagonizes the FcγRIIB receptor
    B. Binds to the FcγRIIB receptor
    C. Delivers inhibitory signals to B lymphocytes and activating signals to myeloid cells
    D. Increases antibody production
A
  1. B, Binds to the FcγRIIB receptor, pg 281.
    IVIG increases expression of FcγRIIB and binds to this receptor. It delivers inhibitory signals to B lymphocytes and myeloid cells leading to decreased antibody production and dampened inflammation.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

40
Q 
4. Which cell type functions to destroy cells coated by antibody?
A. CD4+ T cells
B. Natural killer cells
C. Neutrophils
D. Plasmacytoid DC’s
A
  1. B, Natural killer cells, pg 281.
    Natural killer cells and other leukocytes bind to antibody-coated cells by Fc receptors and destroy these cells through the process of antibody-dependent cell-mediated cytotoxicity (ADCC). ADCC only occurs if the target cell is coated with antibody molecules, as free plasma IgG cannot activate NK cells or compete with cell-bound IgG for binding to FcγRIII.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

41
Q 
5. Deficiencies in the terminal complement proteins (C5-9) predispose to infection by which of the following organisms?
A. Streptococcus
B. Staphylococcus
C. Neisseria
D. Pseudomonas
A
  1. C, Neisseria, pg 296.
    Terminal complement protein deficiency leads to increased infection with N. meningitidis and N. gonorrhoeae. Because of the rarity of some of these infections, some clinicians feel that a single episode of Neisseria meningitis is reason to evaluate for terminal complement deficiency.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

42
Q
  1. Which of the following is an important component of neonatal immunity in the first days to weeks of life?
    A. Maternal IgA and IgG transported through breast milk
    B. Maternal IgM transported through breastmilk
    C. Maternal neutrophils
    D. Vaccines
A
  1. A, Maternal IgA and IgG transported through breast milk, pg 297.
    Maternal antibodies transported across the placenta and in ingested milk protect neonates from infection. IgG is transported across the placenta and maternal IgA and IgG are shared
    via breast milk ingestion. While the infant has mechanisms of innate immunity that are active at birth, these are not directly shared from the mother.

Chapter 13: Effector Mechanisms of Humoral Immunity
Cellular and Molecular Immunology, 9th edition

43
Q
  1. Which of the following is true regarding chemokines in the recruitment of inflammatory cells in allergic disease?
    A. Chemokines do not act in sequence to determine the final inflammatory response so chemokine inhibitors will likely be very effective
    B. Chemokines work through G protein-coupled receptors
    C. The only chemokine receptor for allergic disease is CCR3
    D. The only chemokines that are chemotactic for eosinophils are CCL11 and CCL24
A
  1. B, Chemokines work through G protein-coupled receptors.
    Chemokines do act in sequence in determining the final inflammatory response so inhibitors may not be effective, depending on the kinetics of the response. Examples of chemokines that are chemotactic for eosinophils include: CCL11, CCL24, CCL28, CCL5, and CCL13. CC3 and CC4 are chemokine receptors that can be targeted for their involvement in allergic
    disease.

Chapter 21: Pathophysiology of Allergic Inflammation
Middleton’s Allergy Principles and Practice, 8th Edition

44
Q
  1. During apoptosis, which of the following directly results in release of cytochrome c into the cytoplasm?
    A. Increased lysosomal membrane permeability
    B. Increased mitochondrial membrane permeability
    C. Increased nuclear membrane permeability
    D. Increased plasma membrane permeability
A
  1. B, Increased mitochondrial membrane permeability.
    Cytochrome c is contained in the mitochondria. Certain pro-apoptotic proteins, such as BAX, can translocate into the mitochondria when activated, leading to increased mitochondrial
    membrane permeability and subsequent cytochrome c release.

Chapter 100: Antileukotriene Therapy in Asthma Prepared by: Jackie Eastman Middleton’s Allergy Principles and Practice, 8th Edition

45
Q 
2. Which of the following cytokines increases eosinophil apoptosis?
A. Interleukin-3
B. Interleukin-4
C. Interleukin-5
D. Interleukin-13
A
  1. B, Interleukin-4.
    Interleukin-4 notably increases eosinophil apoptosis, in contrast to most other Th2 cytokines.

Chapter 25: Resolution of Allergic Inflammation
Middleton’s Allergy Principles and Practice, 8th Edition

46
Q 
3. Activation of which of the following receptors leads to eosinophil apoptosis?
A. FAS ligand receptor
B. GM-CSF receptor
C. Interleukin-5 receptor
D. TRAIL
A
  1. A, FAS ligand receptor.
    Activation of the remaining receptors promotes eosinophil survival.

Chapter 25: Resolution of Allergic Inflammation
Middleton’s Allergy Principles and Practice, 8th Edition

47
Q 
1. The 5-lipoxygenase pathway is most abundant in which cell type:
A. Epithelial
B. Lymphoid
C. Myeloid
D. Smooth muscle
A
  1. C, Myeloid, pg 1602.
    Arachidonic acid can be metabolized via various lipoxygenase pathways, depending on the cell type. 5-LO, the one most relevant to asthma, is most abundant in myeloid cells.

Chapter 100: Antileukotriene Therapy in AsthmaPrepared by: Jackie Eastman Middleton’s Allergy Principles and Practice, 8th Edition

48
Q
  1. The function of 5-lipoxygenase (5-LO) activating protein (FLAP) is:
    A. channeling of arachidonic acid to the enzyme 5-LO.
    B. production of arachidonic acid.
    C. transport of 5-LO to the endoplasmic reticulum.
    D. ubiquitination of 5-LO.
A
  1. A, channeling of arachidonic acid to the enzyme 5-LO, pg 1603.
    5-LO activating protein is thought to be required due to its function of channeling arachidonic acid to the enzyme 5-LO. It has no role in 5-LO transport or ubiquitination. Arachidonic acid is metabolized from membrane phospholipids by phospholipase A2.

Chapter 100: Antileukotriene Therapy in Asthma Prepared by: Jackie Eastman Middleton’s Allergy Principles and Practice, 8th Edition

49
Q
  1. Which of the following statements is true about the two cysteinyl leukotriene receptors, CysLT1 and CysLT2?
    A. Both are receptors for leukotriene B4
    B. Leukotriene receptor antagonists block both receptors equally
    C. mRNA for CysLT1 and CysLT2 has been mapped to airway smooth muscle cells
    D. Only CysLT1 is found on mast cells
A
  1. C, mRNA for CysLT1 and CysLT2 have been mapped to airway smooth muscle cells, pg 1603.

Both CysLT2 and CysLT1 have been mapped to airway smooth muscle. LTRAs only antagonize CysLT1. Both receptors are found on mast cells. LTB4 has its own receptors (BLT1 and BLT2).

Chapter 100: Antileukotriene Therapy in Asthma Prepared by: Jackie Eastman Middleton’s Allergy Principles and Practice, 8th Edition

Allergy/Immunology Board Review FIT Corner Questions from Middleton's (15 decks)

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