Student consult questions
55 important questions on Student consult questions
A drug that blocks the function of the chemokine receptor CCR7 would result in which of the following abnormalities?
A. Reduced numbers of T cells in lymph nodes B. Absence of B cell follicles in the spleen
C. Reduced blood neutrophil count
D. Absence of follicular dendritic cells in lymph node follicles
E. Thin thymic cortex
A. Reduced numbers of T cells in lymph nodes
Migration of leukocytes out of the blood into tissues mainly occurs in which type of vessel?
A. Arteries
B. Arterioles
C. Capillaries
D. Venules
E. Veins
D. Venules
Which of the following accurately describe the function of the selectin family of adhesion molecules?
A. Selectins support low affinity rolling of leukocytes on endothelial cells
B. Endothelial selectins increase their affinity for binding to leukocytes in response to chemokines
C. Selectins guide migration of leukocytes though interendothelial junctions
D. Selectins are expressed only on naïve T cells
E. Selectins play a direct role in clonal selection
A. Selectins support low affinity rolling of leukocytes on endothelial cells
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Which of the following is one of the major functions of chemokines in the immune system?
A. Increase affinity of leukocyte selectins for their ligands on endothelial cells.
B. Stimulate proliferation of B cells in response to antigen
C. Increase vascular permeability during the innate immune response to microbes
D. Maintain the spatial separation of B and T lymphocytes within lymphoid tissues E. Form pores in bacterial membranes
D. Maintain the spatial separation of B and T lymphocytes within lymphoid tissues
Which of the following is not a function of the innate immune system?
A. Rapidly respond to microbial infections by promoting acute inflammation
B. Respond to viral infections by inducing the expression of type I interferons
C. Respond to microbial infections by inducing expression of T cell costimulators on antigen presenting cells D. Respond to damaged and dying host cells by inducing acute inflammation E. Respond to microbial infections by inducing a state of long lived memory that prevents repeat infections by the same microbe
E.Respond to microbial infections by inducing a state of long lived memory that prevents repeat infections by the same microbe
Which of the following is a proinflammatory cytokine of major importance in innate immunity that has been successfully targeted by drugs to treat rheumatoid arthritis (RA)?
A. Tumor necrosis factor (TNF)
B. Transforming growth factor-β (TGF-β) C. Interleukin 10 D. Interleukin 2 E. Interferon γ
A. Tumor necrosis factor (TNF)
Toll like receptors (TLRs) located in endosomal membranes of cells recognize which of the following?
A. Nucleic acids
B. Bacterial cell wall lipotechoic acid
C. Bacterial cell wall lipopolysaccharide
D. Uric acid crystals
E. Peptides containing N-formylmethionyl residues
A. Nucleic acids
All of the following molecules are opsonins that facilitate efficient phagocytosis of microbes by neutrophils and macrophages EXCEPT:
A. C3b
B. C5a
C. C-reactive protein
D. IgG
E. Mannose-binding lectin
B. C5a
Which of the following is a feature of Natural Killer (NK) cells?
A. They express antigen receptors that directly bind antigens on the surface of microbes
B. They are activated by recognizing microbial peptides bound to host class I MHC molecules
C. They kill virally infected cells by a perforin/granzyme dependent mechanism
D. Upon activation, they secrete abundant interleukin-4
E. They secrete natural IgM antibodies
C. They kill virally infected cells by a perforin/granzyme dependent mechanism
Monoclonal antibodies used as drugs or diagnostic reagents are characterized by all of the following EXCEPT:
A. Single antigen specificity
B. Production vy a B cell hybridoma
C. Single isotype
D. Monovalent, with one antigen-binding site
E. Known antigen specificity
D. Monovalent, with one antigen-binding site
Monoclonal antibodies are, by definition, identical antibodies of a single isotype and antigen specificity, produced by a single clone of cells. They are usually produced in vitro by clonal B cell hybridomas and are structurally normal, with at least two antigen-binding sites and a known specificity. Tumors of B lymphocytes (e.g., myelomas) may produce monoclonal antibodies, usually of unknown specificity, or often single chains of antibody molecules.
Monoclonal antibodies are, by definition, identical antibodies of a single isotype and antigen specificity, produced by a single clone of cells. They are usually produced in vitro by clonal B cell hybridomas and are structurally normal, with at least two antigen-binding sites and a known specificity. Tumors of B lymphocytes (e.g., myelomas) may produce monoclonal antibodies, usually of unknown specificity, or often single chains of antibody molecules.
Which one of the following is a correct description of the basic symmetric core structure of an IgG antibody?
A. One heavy chain and two light chains
B. One constant domain and one variable domain.
C. Two heavy chains and one light chain
D. Two heavy chains and two light chains
E. One heavy chain and one light chain
D. Two heavy chains and two light chains
An antigen-binding site of an IgG antibody molecule is composed of which of the following?
A. Twelve hypervariable loops, three each on two heavy chains and two light chains
B. Three hypervariable loops on a light chain
C. Three hypervariable loops on a heavy chain
D. Six hypervariable loops, three each on one heavy chain and one light chain
E. Six hypervariable loops, three each on two heavy chains
D. Six hypervariable loops, three each on one heavy chain and one light chain
An IgG molecule has two antigen binding sites. Each one is composed of six hypervariable loops, three that extend from the variable domains of a heavy chain and three that extend from the variable domains of the covalently linked light chain.
An IgG molecule has two antigen binding sites. Each one is composed of six hypervariable loops, three that extend from the variable domains of a heavy chain and three that extend from the variable domains of the covalently linked light chain.
Which of the following properties of antibodies is not related to isotype?
A. Ability to activate complement
B. Ability to act as an opsonin for phagocytosis of antigens
C. Antigen specificity D. Ability to be transported into the lumen of the gut E. Ability to activate mast cells
C. Antigen specificity
Which of the following is the nonpolymorphic molecule that is structurally homologous to the class I MHC α chain, associates with β2-microglobulin, and displays lipid antigens for recognition by NKT cells?
A. CD1
B. CD2
C. CD3
D. CD4
E. CD8
A. CD1
CD1 is encoded outside the MHC, but is structurally homologous to class I MHC molecules. Some subsets of T cells, all with relatively invariant T cell receptors, recognize lipid or glycolipid antigens bound to CD1 on antigen-presenting cells. CD2, CD3, CD4, and CD8 are all present on T cells. Although they are members of the Ig superfamily, like class I MHC, they are not otherwise homologous to class I MHC and do not bind and display antigens for T cell recognition.
CD1 is encoded outside the MHC, but is structurally homologous to class I MHC molecules. Some subsets of T cells, all with relatively invariant T cell receptors, recognize lipid or glycolipid antigens bound to CD1 on antigen-presenting cells. CD2, CD3, CD4, and CD8 are all present on T cells. Although they are members of the Ig superfamily, like class I MHC, they are not otherwise homologous to class I MHC and do not bind and display antigens for T cell recognition.
Which of the following is a human class I MHC molecule?
A. HLA-DR
B. HLA-DP
C. HLA-B
D. I-A
E. CD8
C. HLA-B
The human class I MHC molecules are HLA-A, HLA-B, and HLA-C. The human class II MHC molecules are HLA-DP, HLA-DQ, and HLA-DR. I-A is a mouse class II MHC molecule. CD8 is not an MHC molecule, but it binds to class I MHC molecules.
The human class I MHC molecules are HLA-A, HLA-B, and HLA-C. The human class II MHC molecules are HLA-DP, HLA-DQ, and HLA-DR. I-A is a mouse class II MHC molecule. CD8 is not an MHC molecule, but it binds to class I MHC molecules.
In the class I MHC pathway of antigen presentation, peptides generated in the cytosol are translocated into the endoplasmic reticulum in which of the following ways?
A. By ATP-dependent transport via TAP
B. By passive diffusion
C. By receptor-mediated endocytosis
D. Through membrane pores
E. Via the proteasome
A. By ATP-dependent transport via TAP
The TAP1/TAP2 heterodimer is an ATP-dependent pump that delivers peptides generated by the proteasome into the endoplasmic reticulum.
The TAP1/TAP2 heterodimer is an ATP-dependent pump that delivers peptides generated by the proteasome into the endoplasmic reticulum.
In the class I MHC pathway of antigen presentation, cytoplasmic proteins are tagged for proteolytic processing by covalent linkage with which of the following molecules?
A. Calreticulin
B. Nuclear factor (NF)-κB
C. Tapasin
D. Ubiquitin
E. Calnexin
D. Ubiquitin
In the class I pathway, proteins are tagged for proteasomal processing by covalent addition of several copies of the polypeptide ubiquitin. Ubiquitin-dependent proteasomal proteolysis is also important in many other cellular processes besides antigen presentation. For example, NF-κB is a transcription factor whose activation is dependent on ubiquitination and proteasomal degradation of an inhibitor (called IκB). Calreticulin, tapasin, and calnexin regulate the assembly of class I MHC proteins within the endoplasmic reticulum.
In the class I pathway, proteins are tagged for proteasomal processing by covalent addition of several copies of the polypeptide ubiquitin. Ubiquitin-dependent proteasomal proteolysis is also important in many other cellular processes besides antigen presentation. For example, NF-κB is a transcription factor whose activation is dependent on ubiquitination and proteasomal degradation of an inhibitor (called IκB). Calreticulin, tapasin, and calnexin regulate the assembly of class I MHC proteins within the endoplasmic reticulum.
MHC genes are the most polymorphic of any in the human genome. Which of the following statements about MHC polymorphism is true?
A. HLA-A, HLA-B, and HLA-C represent three different alleles of the same gene.
B. Many unrelated people have identical MHC alleles
C. Only class I MHC genes are polymorphic; class II MHC genes are not.
D. Most of the polymorphic residues in any MHC protein are located in the peptide binding groove
E. MHC polymorphism is a result of somatic recombination of inherited nonpolymorphic MHC gene segments
D. Most of the polymorphic residues in any MHC protein are located in the peptide binding groove
The required number of complexes of a microbial peptide and a particular class II MHC allele on the surface of an antigen-presenting cell to initiate a T cell response specific for the viral peptide is:
A. One
B. All the MHC molecules on the cell must be complexed with the peptide
C. About 0.1% of the total number of class II MHC molecules on the cell surface
D. Greater than 10^6
E. Zero
C. About 0.1% of the total number of class II MHC molecules on the cell surface
As few as 100 complexes of a particular peptide and a particular class II MHC molecule are needed to activate naive T cells specific for that complex and thereby initiate a detectable T cell response. This represents less than 0.1% of the total class II MHC molecules on a typical antigen-presenting cell surface.
As few as 100 complexes of a particular peptide and a particular class II MHC molecule are needed to activate naive T cells specific for that complex and thereby initiate a detectable T cell response. This represents less than 0.1% of the total class II MHC molecules on a typical antigen-presenting cell surface.
Which of the following is an example of G protein-coupled receptor (GPCR)?
A. T cell antigen receptor (TCR)
B. B cell antigen receptor (BCR)
C. CD4
D. Interlukin-2 (IL-2) receptor
E. Chemokinereceptor CCR7
E. Chemokinereceptor CCR7
The cytoplasmic tails of the signaling polypeptides found in lymphocyte antigen receptor complexes (BCR and TCR) contain regions that become phosphorylated upon antigen recognition and then bind ZAP family kinases. These regions are called:
A. Immunoreceptor tyrosine-based activating motifs (ITAMs)
B. Fc regions
C. Toll-like IL-1R (TIR) domains
D. Complementarity determining regions
E. Nod like receptor (NLR) domains
A. Immunoreceptor tyrosine-based activating motifs (ITAMs)
In the T cell calcium signaling pathway induced by antigen recognition, which enzyme and transcription factor are activated?
A. IκB kinase, NFκB
B. Jun kiniase (JNK), AP-1
C. Erk kinase, Fos
D. JAK3, STAT4
E. Calcineurin, NFAT
E. Calcineurin, NFAT
In the cannonical NF-κB signaling pathway downstream of the TNF receptor, TLRs, and antigen receptors, what role does IκB kinase (IKK) complex play?
A. IKK enters the nucleus and phosphorylates NF-κB that has bound to the promoters of proinflammatory genes
B. IKK binds to NF-κB, preventing it from entering the nucleus
C. Activated IKK phosphorylates IκBα, which leads to IκBα degradation, allowing NF-κB to enter the nucleus
D. IKK enters the nucleus and binds to the promoters of pro inflammatory genes
E. IKK phosphorylates NFκB, allowing NF-κB to enter the nucleus
C. Activated IKK phosphorylates IκBα, which leads to IκBα degradation, allowing NF-κB to enter the nucleus
A one year old boy with a history of severe infections is found to have very few circulating mature T cells or NK cells, but normal numbers of B cells. Genetic studies reveal he has X-linked severe combined immunodeficiency syndrome. Defective signaling by the receptor for which cytokine is the underlying cause of this disease?
A. IL-1
B. IL-2
C. IL-4
D. IL-7
E. GM-CSF
D. IL-7
X-linked severe combined immunodeficiency syndrome (X-linked SCID) caused by mutations in the common γ chain which is a signaling polypeptide in the multimeric cytokine receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. Although signaling from all of these receptors would be defective in X-linked SCID, only IL-7 is required for early development of T cells and NK cells in the thymus of humans.
X-linked severe combined immunodeficiency syndrome (X-linked SCID) caused by mutations in the common γ chain which is a signaling polypeptide in the multimeric cytokine receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. Although signaling from all of these receptors would be defective in X-linked SCID, only IL-7 is required for early development of T cells and NK cells in the thymus of humans.
Which enzyme contributes to antigen receptor junctional diversity by adding random nucleotides at the junctions between V, D, and J segments and is also useful as a marker of neoplasia of pro-B and pro-T cells?
A. Terminal deoxyribonucleotidyl transferase (TdT)
B. Activation-induced deaminase (AID)
C. Recombinase activating gene-1 (RAG-1)
D. DNA-dependent protein kinase
E. DNA polymerase
A. Terminal deoxyribonucleotidyl transferase (TdT)
Which of the following mechanisms accounts for the fact that all of the TCRs produced by a single T cell have identical β chains?
A. X inactivation
B. Light chain isotype exclusion
C. Antigen receptor gene homozygosity
D. Linkage disequilibrium
E. Allelic exclusion
E. Allelic exclusion
In TCR allelic exclusion, expression of the β chain gene encoded by a successfully recombined gene on one chromosome inhibits recombination of the β chain gene on the other chromosome. The inhibitory signals are generated by the pre-TCR. This ensures that the T cell will not produce receptors with two different β chains. However, allelic exclusion does not occur for TCR α chain genes, and many T cells may express TCRs with two different α chains. Heavy chain allelic exclusion occurs by a similar mechanism in B cell development.
In TCR allelic exclusion, expression of the β chain gene encoded by a successfully recombined gene on one chromosome inhibits recombination of the β chain gene on the other chromosome. The inhibitory signals are generated by the pre-TCR. This ensures that the T cell will not produce receptors with two different β chains. However, allelic exclusion does not occur for TCR α chain genes, and many T cells may express TCRs with two different α chains. Heavy chain allelic exclusion occurs by a similar mechanism in B cell development.
Most naïve T cell activation occurs where and in response to what?
A. In the skin in response to cytokines
B. In the infected tissues in response to antigen presentation by macrophages
C. In the blood in response to antigen presentation by monocytes
D. In the thymus in response to antigen presentation by thymic medullary epithelial cells
E. In secondary lymphoid organs in response to antigen presentation by dendritic cells
E. In secondary lymphoid organs in response to antigen presentation by dendritic cells
The most important costimulators for naïve T cell activation are which of the following?
A. ICOS ligand
B. B7-1 and B7-2
C. PD-L1 and PD-L2
D. OX40-ligand
E. FAS ligand
B. B7-1 and B7-2
B7-1 (CD80) and B7-2 (CD86) are the major costimulators required for naïve T cell activation. They are expressed on mature myeloid DCs, and bind to CD28 on the T cells. ICOS-Ligand and OX40 ligand are costimulators for previously activated T cells; their receptors are not expressed on naïve T cells. PD-L1 and PD-L2 bind to PD-1 on T cells, which inhibits T cell activation. FAS Ligand binds to FAS on T cells, and induces apoptotic cell death.
B7-1 (CD80) and B7-2 (CD86) are the major costimulators required for naïve T cell activation. They are expressed on mature myeloid DCs, and bind to CD28 on the T cells. ICOS-Ligand and OX40 ligand are costimulators for previously activated T cells; their receptors are not expressed on naïve T cells. PD-L1 and PD-L2 bind to PD-1 on T cells, which inhibits T cell activation. FAS Ligand binds to FAS on T cells, and induces apoptotic cell death.
The combination of TCR and costimulatory signals induces naïve T cells to express IL-2 and high affinity IL-2 receptors. This results in which of the following functional responses by the T cell?
A. Clonal expansion
B. Interferon γ expression
C. CD40 ligand expression
D. Granule exocytosis
E. Migration out of a lymph node
A. Clonal expansion
At the peak of a CD8+ T cell response to a new microbe, what is the fold increase in the number of microbe-specific T cells in an individual compared to the number of naïve CD8+ T cells specific for the microbe before infection?
A. ~100
B. ~1.000
C. ~10.000
D. ~100.000
D. ~10.0000
CD8+ T cells undergo tremendous clonal expansion in response to antigen stimulation. CD4+ clonal expansion is less, on the order of 1000 to 10,000 fold
CD8+ T cells undergo tremendous clonal expansion in response to antigen stimulation. CD4+ clonal expansion is less, on the order of 1000 to 10,000 fold
TH2 cells are defined in part by production of which of the following cytokines?
A. TNF
B. IL-1
C. IL-2
D. IL-4
E. IFNgamma
D. IL-4
TH1 cells are defined by production of IFNγ. TH2 cells are defined by production of IL-4, IL-5, and IL-13. TH17 cells are defined by production of IL-17A, IL-17F, and IL-22. Many T cells produce combinations of various cytokines, and polarized cells expressing restricted cytokine profiles tend to develop upon chronic or repeated stimulation.
TH1 cells are defined by production of IFNγ. TH2 cells are defined by production of IL-4, IL-5, and IL-13. TH17 cells are defined by production of IL-17A, IL-17F, and IL-22. Many T cells produce combinations of various cytokines, and polarized cells expressing restricted cytokine profiles tend to develop upon chronic or repeated stimulation.
The differentiation of each major CD4+ T cell subset is controlled by a subset defining transcription factor. Which of the following correctly pairs each subset with its transcription factor?
A. TH1:T-bet; TH2:GATA3; TH17:RORγT
B. TH1:GATA3; TH2:T-bet; TH17:RORγT
C. TH1:T-bet; TH2: RORγT; TH17: GATA3
D. TH1: RORγT; TH2:GATA3; TH17: T-bet
E. TH1: GATA3; TH2:RORγT; TH17: T-bet
A. TH1:T-bet; TH2:GATA3; TH17:RORγT
T-bet, GATA3, and RORγT are sometimes called “master regulators”, and they are required for differentiation and function of the differentiated T cells. In each case the transcription of the subset defining cytokine genes is regulated by the subset defining transcription factors. Other transcription factors are also required for the differentiation of each subset.
T-bet, GATA3, and RORγT are sometimes called “master regulators”, and they are required for differentiation and function of the differentiated T cells. In each case the transcription of the subset defining cytokine genes is regulated by the subset defining transcription factors. Other transcription factors are also required for the differentiation of each subset.
A major function of TH1 cells is to activate macrophages. Which molecules expressed by TH1 cells are essential for this function?
A. IL-1 and TNF
B. CD8 and Fas ligand
C. IL-17 and NO
D. Interferon gamma and CD40 ligand
E. IL-4 and ICOS
D. Interferon gamma and CD40 ligand
TH1 cells activate macrophages via secreted interferon γ and membrane CD40 ligand, which bind respectively to interferon γ receptors and CD40 on the macrophages. TH1 cells express CD4 and not CD8. Although TH1 cells express Fas ligand, this molecule does not activate macrophages, but rather binds to Fas on various cell types and induces apoptotic cell death. IL-17 and NO are not made by TH1 cells. IL-4 is not made by TH1 cells, and ICOS does not activate macrophages.
TH1 cells activate macrophages via secreted interferon γ and membrane CD40 ligand, which bind respectively to interferon γ receptors and CD40 on the macrophages. TH1 cells express CD4 and not CD8. Although TH1 cells express Fas ligand, this molecule does not activate macrophages, but rather binds to Fas on various cell types and induces apoptotic cell death. IL-17 and NO are not made by TH1 cells. IL-4 is not made by TH1 cells, and ICOS does not activate macrophages.
Activated macrophages perform all of the following functions EXCEPT:
A. Inhibition of fibroblast proliferation and angiogenesis within damaged tissues
B. Production of lysosomal enzymes and reactive oxygen species that kill phagocytosed microbes
C. Presentation of antigen to helper T cells
D. Secretion of inflammatory cytokines such as tumor necrosis factor and interleukin-1
E. Production of nitric oxide, which helps kill microorganisms
A. Inhibition of fibroblast proliferation and angiogenesis within damaged tissues
Which of the following is one way a cytokine made by TH2 cells contributes to atopic disease (allergy)?
A. IL-17 stimulates TNF production by macrophages
B. IL-5 activates eosinophils
C. IL-13 activates macrophages to produce nitric oxide
D. IL-4 induces B cell class switching to IgA
E. IL-22 causes mast cell degranulation
E. IL-22 causes mast cell degranulation
Atopic diseases often involve eosinophil activation and the release of pro-inflammatory and tissue damaging granule contents, such as major basic protein. TH2 cells underlie these events because they produce IL-5. IL-17and IL-22 are not made by TH2 cells. IL-13 does not activate macrophages to produce nitric oxide. IL-4 does induces B cell class switching to IgE not IgA
Atopic diseases often involve eosinophil activation and the release of pro-inflammatory and tissue damaging granule contents, such as major basic protein. TH2 cells underlie these events because they produce IL-5. IL-17and IL-22 are not made by TH2 cells. IL-13 does not activate macrophages to produce nitric oxide. IL-4 does induces B cell class switching to IgE not IgA
Alternative macrophage activation is characterized by which one of the following?
A. Reactive oxygen species (ROS) generation
B. IL-1 production
C. Microbial killing
D. IL-10 and TGF beta secretion
E. IL-4 and IL-13 secretion
D. IL-10 and TGF beta secretion
Alternatively activated macrophages secrete the anti-inflammatory cytokines IL-10 and TGFβ. They also enhance angiogenesis and fibrosis. ROS generation, IL-1, and microbial killing are characteristic of classically activated macrophages. IL-4 and IL-13 are cytokines made by TH2 cells, which induce alternative macrophage activation
Alternatively activated macrophages secrete the anti-inflammatory cytokines IL-10 and TGFβ. They also enhance angiogenesis and fibrosis. ROS generation, IL-1, and microbial killing are characteristic of classically activated macrophages. IL-4 and IL-13 are cytokines made by TH2 cells, which induce alternative macrophage activation
Which type of T cell is most likely to promote acute neutrophillic inflammatory responses that defend against extracellular bacteria and fungi?
A. Th1
B. Th2
C. Th17
D. CTL
E. T follicular helper
C. Th17
IL-17 produced by TH17 cells induces many cell types to make chemokines such as IL-8, and cytokines such as IL-1 and TNF, all of which enhance neutrophil recruitment into tissues. TH1 cells and CTLs, which secrete IFNγ, are more typically associated with chronic inflammatory infiltrates rich in activated macrophages, and TH2 cells are associated with eosinophil-rich inflammation. T follicular helper cells do not promote inflammatory responses, but rather help B cells in germinal center reactions.
IL-17 produced by TH17 cells induces many cell types to make chemokines such as IL-8, and cytokines such as IL-1 and TNF, all of which enhance neutrophil recruitment into tissues. TH1 cells and CTLs, which secrete IFNγ, are more typically associated with chronic inflammatory infiltrates rich in activated macrophages, and TH2 cells are associated with eosinophil-rich inflammation. T follicular helper cells do not promote inflammatory responses, but rather help B cells in germinal center reactions.
Which of the following is a property of exhausted CD8+ T cells?
A. Low expression of CTLA-4
B. High expressing of IL-4
C. High expression of PD-1
D. Low expression of class I MHC
E. High expression of interferon-gamma
C. High expression of PD-1
Exhausted CD8+ CTL arise when there is persistent exposure to antigen, such as in the setting of chronic infections or cancers. Exhausted CTLs have high expression of the inhibitory receptor PD-1 and other inhibitory molecules such as CTLA-4. Exhausted T cells produce less interferon-γ than normal CTL. CTL do not express IL-4, and class I MHC expression is not typically altered.
Exhausted CD8+ CTL arise when there is persistent exposure to antigen, such as in the setting of chronic infections or cancers. Exhausted CTLs have high expression of the inhibitory receptor PD-1 and other inhibitory molecules such as CTLA-4. Exhausted T cells produce less interferon-γ than normal CTL. CTL do not express IL-4, and class I MHC expression is not typically altered.
CTLs are the major defense against which of the following class of organisms?
A. Extracellular bacteria
B. Fungi
C. Protozoans
D. Viruses
E. Helminths
D. Viruses
A child born with homozygous mutations in a gene required for T follicular helper cell differentiation will be able to make antibodies against which of the following antigens?
A. Tetanus toxoid
B. Influenza hemagglutinin
C. Bee venom proteins
D. ABO blood group antigens
E. Rh factor antigen
D. ABO blood group antigens
T cell–independent antigens include polysaccharides, glycolipids and nucleic acids with multiple repeated epitopes, which may cross-link the B cell receptor maximally and thus bypass the need for T cell help. Of the choices given, the best choice is the ABO blood group antigen, because of its polyvalent glycolipid structure. The other antigens are all proteins, antibody responses to which require T cell help, including help from T follicular helper cells.
T cell–independent antigens include polysaccharides, glycolipids and nucleic acids with multiple repeated epitopes, which may cross-link the B cell receptor maximally and thus bypass the need for T cell help. Of the choices given, the best choice is the ABO blood group antigen, because of its polyvalent glycolipid structure. The other antigens are all proteins, antibody responses to which require T cell help, including help from T follicular helper cells.
Which of the following membrane proteins on a B cell generate inhibitory signals that block proliferation and differentiation of the B cell?
A. FcgammaRIIB
B. TLR5
C. CR2/CD21
D. Membrane IgM
E. CD40
A. FcgammaRIIB
Antibody feedback is the mechanism of regulation of humoral immune responses and is mediated by the FcγRIIB receptor, which delivers inhibitory signals into the B cells on binding the Fc portion of IgG. Each of the other proteins listed generate B cell activating signals.
Antibody feedback is the mechanism of regulation of humoral immune responses and is mediated by the FcγRIIB receptor, which delivers inhibitory signals into the B cells on binding the Fc portion of IgG. Each of the other proteins listed generate B cell activating signals.
The germinal center reaction generates long lived plasma cells which secrete protective high affinity B cells for many years. Where do these cells reside?
A. Bone marrow
B. Thymus
C. Parathyroid
D. Skin
E. Splenic red pulp
A. Bone marrow
Plasmablasts generated in the germinal center migrate to the bone marrow, and differentiate into long-lived plasma cells, which remain active antibody secreting cells for months to years.
Plasmablasts generated in the germinal center migrate to the bone marrow, and differentiate into long-lived plasma cells, which remain active antibody secreting cells for months to years.
Which of the following is NOT true about heavy chain isotype switching?
A. It is induced by recombination of Ig constant region DNA segments
B. It is defective in individuals lacking functional CD40 or CD40-ligand
C. It is prominent in antibody responses to polysaccharides
D. It generates antibodies with diverse effector functions
E. Is induced by the AID, the enzyme that is also involved in somatic mutation of Ig V genes
C. It is prominent in antibody responses to polysaccharides
Isotype switching requires signals from helper T cells, so it is most prominent in antibody responses to protein antigens and not T-independent polysaccharides. The molecular mechanism does involve “switch recombination” of Ig gene segments, which is stimulated by CD40L-CD40 interactions and AID. Antibodies of different ispotypes serve distinct functions.
Isotype switching requires signals from helper T cells, so it is most prominent in antibody responses to protein antigens and not T-independent polysaccharides. The molecular mechanism does involve “switch recombination” of Ig gene segments, which is stimulated by CD40L-CD40 interactions and AID. Antibodies of different ispotypes serve distinct functions.
Which of the following functions of antibodies does NOT require Fc receptors specific for IgG?
A. Phagocytosis of antibody opsonized antigens by neutrophils
B. Antibody mediated cellular cytotoxicity by NK cells
C. Antibody mediated feedback inhibition of B cells
D. Neonatal immunity mediated by maternal antibodies transported through the placenta
E. Neutralization of tetanus toxin by anti-tetanus antibodies
E. Neutralization of tetanus toxin by anti-tetanus antibodies
Neutralization of microbes and toxins requires binding of antibody and no other effector functions. Neutrophils and macrophages utilize IgG Fc receptors (FcγR1 and FcγRII) to phagocytose IgG-opsonized antigens. Antibody feedback inhibition of B cells is mediated by FcγRIIB on the B cell. Neonatal immunity depends on transplacental transport of IgG via the neonatal Fc receptor (FcRn)
Neutralization of microbes and toxins requires binding of antibody and no other effector functions. Neutrophils and macrophages utilize IgG Fc receptors (FcγR1 and FcγRII) to phagocytose IgG-opsonized antigens. Antibody feedback inhibition of B cells is mediated by FcγRIIB on the B cell. Neonatal immunity depends on transplacental transport of IgG via the neonatal Fc receptor (FcRn)
The immune system associated with mucosal tissues includes organized lymphoid structures where specialized adaptive immune responses are initiated. Which of the following is not included in mucosal associated lymphoid tissues?
A. Tonsils
B. Peyer's patches
C. Axillary lymph nodes
D. Mesenteric lymph nodes
E. Adenoids
C. Axillary lymph nodes
Axillary lymph nodes drain the skin and soft tissues of the upper extremities, and not mucosal tissues. Tonsils and adenoids are sites of adaptive immune responses to microbes in the oral cavity and pharynx. Peyer's patches and mesenteric nodes are sites of initiation of adaptive immune responses to microbes in the gut.
Axillary lymph nodes drain the skin and soft tissues of the upper extremities, and not mucosal tissues. Tonsils and adenoids are sites of adaptive immune responses to microbes in the oral cavity and pharynx. Peyer's patches and mesenteric nodes are sites of initiation of adaptive immune responses to microbes in the gut.
What are M cells?
A. A type of mucosal B cell that secretes IgM
B. Lamina propria macrophages that ingest bacteria that have invaded through the intestinal epithelium
C. Alveolar macrophage that secrete surfactant
D. Specialized intestinal epithelial cells that transport antigens or microbes into Peyer's patches
E. A type of intestinal dendritic cell that tolerizes T cells to food antigens.
D. Specialized intestinal epithelial cells that transport antigens or microbes into Peyer's patches
M cells are intestinal epithelial cells with short villi, and engage in transport of intact microbes or molecules across the mucosal barrier into gut-associated lymphoid tissues, such as Peyer's patches, where they are handed off to DCs
M cells are intestinal epithelial cells with short villi, and engage in transport of intact microbes or molecules across the mucosal barrier into gut-associated lymphoid tissues, such as Peyer's patches, where they are handed off to DCs
The human skin contains about 10 billion T cells. Most of these T cells have which of the following phenotypes?
A. Memory T cells
B. Naïve T cells
C. Th17 cell
D. Regulatory T cells
E. CD8+ T cells
A. Memory T cells
Most of the skin T cells are in the dermis, and have an effector memory phenotype. They are a mixture of CD4+ and CD8+ T cells.
Most of the skin T cells are in the dermis, and have an effector memory phenotype. They are a mixture of CD4+ and CD8+ T cells.
Which of the following is NOT a consequence of recognition of self antigens by developing lymphocytes
A. Apoptosis (clonal deletion) of T cells in the thymus
B. Apoptosis (clonal deletion) of B cells in the bone marrow
C. Differentiation of Th2 cells
D. Receptor editing in immature B cells
E. Development of regulatore T cells
C. Differentiation of Th2 cells
TH2 cells are a type of effector T cell that differentiates from naïve T cells in peripheral lymphoid tissues, in response to foreign antigens. All the other choices are mechanisms of central tolerance that occur in bone marrow (for B cells) or thymus (for T cells).
TH2 cells are a type of effector T cell that differentiates from naïve T cells in peripheral lymphoid tissues, in response to foreign antigens. All the other choices are mechanisms of central tolerance that occur in bone marrow (for B cells) or thymus (for T cells).
Which of the following is NOT a property of regulatory T cells (Treg)?
A. Interleukin-2 receptor (CD25) expression
B. Secretion of interferon-γ
C. FoxP3 expression
D. Secretion of transforming growth factor-β
E. Inhibition of activation of effector T cells
B. Secretion of interferon-γ
Most Teg are CD4+CD25+ T cells that express the FoxP3 transcription factor, and secrete TFGβ. Interferon γ is an inflammatory cytokine secreted by effector T cells, including TH1 cells and cytotoxic T lymphocytes.
Most Teg are CD4+CD25+ T cells that express the FoxP3 transcription factor, and secrete TFGβ. Interferon γ is an inflammatory cytokine secreted by effector T cells, including TH1 cells and cytotoxic T lymphocytes.
Which one of the following factors generally favors tolerance to an antigen and not stimulation of an immune response?
A. High doses of antigen
B. Short-lived persistence of antigen
C. Cutaneous portal of entry
D. Presence of adjuvant
E. Costimulator expression on antigen-presenting cells
A. High doses of antigen
High doses of antigens, especially administered without adjuvants, favor peripheral tolerance, often by the induction of anergy or apoptosis. Antigens that induce immune responses are typically present for short durations, and are associated with adjuvants that enhance antigen presentation and costimulatory molecule expression.
High doses of antigens, especially administered without adjuvants, favor peripheral tolerance, often by the induction of anergy or apoptosis. Antigens that induce immune responses are typically present for short durations, and are associated with adjuvants that enhance antigen presentation and costimulatory molecule expression.
It has been postulated that regulatory T cells reduce available B7 costimulators on APCs, and this is one possible mechanism by which the Tregs inhibit immune responses. Which of the following molecules is expressed on regulatory T cells (Treg) and functions to block B7-mediated costimulation.
A. PD-1
B. CTLA-4
C. CD28
D. CC127 (IL-7 receptor)
E. Fas ligand
B. CTLA-4
Treg express CTLA-4, and CTLA-4 is a high affinity receptor for B7-1 and B7-2. Treg function depends on CTLA-4, and it is likely that one mechanism of Trge suppression of effector T cell responses is to competitively bind B7-1 and B7-2 on dendritic cells presenting self antigens to naïve T cells, or remove B7 molecules from these APCs. This results in reduced costimulation, which would prevent the induction of effective immune responses.
Treg express CTLA-4, and CTLA-4 is a high affinity receptor for B7-1 and B7-2. Treg function depends on CTLA-4, and it is likely that one mechanism of Trge suppression of effector T cell responses is to competitively bind B7-1 and B7-2 on dendritic cells presenting self antigens to naïve T cells, or remove B7 molecules from these APCs. This results in reduced costimulation, which would prevent the induction of effective immune responses.
Among the genes that are associated with common autoimmune diseases, the strongest associations are with which of the following?
A. Cytokine genes
B. Autophagy genes
C. Apoptosis genes
D. MHC genes
E. Antigen receptor signaling genes
D. MHC genes
MHC genes, mainly class II MHC genes, are the most strongly associated with autoimmune diseases.
MHC genes, mainly class II MHC genes, are the most strongly associated with autoimmune diseases.
Which of the following is NOT part of the innate immune response to extracellular bacteria?
A. Complement activation by peptidoglycan
B. Complement activation by mannose
C. Activation of phaocytes by Toll-like receptors
D. Bacterial killing by natural killer (NK) cells
E. Acute inflammation
D. Bacterial killing by natural killer (NK) cells
Although natural killer cells are part of the innate immune system, they kill infected cells, not extracellular organisms. Innate immune responses to extracellular bacteria include both the alternative complement pathway (activated by peptidoglycan and lipopolysaccharide) and the lectin pathway (activated by mannose-binding lectin). Activation of phagocytes by Toll-like receptors and acute inflammation are key components of the innate immune response to extracellular bacteria.
Although natural killer cells are part of the innate immune system, they kill infected cells, not extracellular organisms. Innate immune responses to extracellular bacteria include both the alternative complement pathway (activated by peptidoglycan and lipopolysaccharide) and the lectin pathway (activated by mannose-binding lectin). Activation of phagocytes by Toll-like receptors and acute inflammation are key components of the innate immune response to extracellular bacteria.
Which type of T cell is most important for defense against extracellular bacteria and fungi?
A. Th1
B. Th2
C. Th17
D. Cytotoxic T lymphocyte
E. NKT cell
C. Th17
Activated TH17 cells simulate acute inflammatory responses with neutrophil rich infiltrates. These responses protect against extracellular microbes. Patients with defects in TH17 differentiation suffer from mucocutaneous candidiasis and recurrent Staphylococcus aureus infections.
Activated TH17 cells simulate acute inflammatory responses with neutrophil rich infiltrates. These responses protect against extracellular microbes. Patients with defects in TH17 differentiation suffer from mucocutaneous candidiasis and recurrent Staphylococcus aureus infections.
Which of the following microbes induces two forms of disease, depending on the genetics of the host, one form characterized by weak cell mediated immunity and widespread proliferation of the microbe in macrophages, and the second form characterized by strong cell mediated immunity and destructive granulomatous inflammation?
A. Candida albicans
B. Vibrio cholerae
C. Corynebacterium diptheriae
D. Epstein Barr virus
E. Mycobacterium leprae
E. Mycobacterium leprae
Mycobacterium leprae cause leprosy. In lepromatous leprosy, patients mount weak cell-mediated responses to M. leprae antigens, and the bacteria proliferate within macrophages and cause destructive lesions in the skin and underlying tissue. In tuberculoid leprosy there is strong T cell-mediated immunity with granulomas that damage sensory nerves. Patients with the tuberculoid form of leprosy produce IFN-γ and IL-2 in lesions (indicative of TH1 cell activation), while patients with lepromatous leprosy produce less IFN-γ and sometimes more IL-4 and IL-10 (suggestive of TH2 cells).
Mycobacterium leprae cause leprosy. In lepromatous leprosy, patients mount weak cell-mediated responses to M. leprae antigens, and the bacteria proliferate within macrophages and cause destructive lesions in the skin and underlying tissue. In tuberculoid leprosy there is strong T cell-mediated immunity with granulomas that damage sensory nerves. Patients with the tuberculoid form of leprosy produce IFN-γ and IL-2 in lesions (indicative of TH1 cell activation), while patients with lepromatous leprosy produce less IFN-γ and sometimes more IL-4 and IL-10 (suggestive of TH2 cells).
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