Exam 1: Practice Set 3 Flashcards
A 26-year-old obstetric patient becomes ill during the first trimester of pregnancy with fever and lymphadenopathy. She is found to have a rising titer of anti-Toxoplasma gondii antibodies. She delivers a full-term baby with no apparent signs of in utero infection. The best test to diagnose acute infection in the neonate (a newborn infant less than four weeks old) would be a parasite-specific ELISA for which isotype of immunoglobulins? A. IgA B. IgD C. IgE D. IgG E. IgM
E. IgM
An antibody preparation is being used in a laboratory protocol to study B cell. The preparation doesn’t activate the cells or cause crosslinking. It doesn’t cause precipitation of its purified ligand, and it doesn’t cause agglutination of latex beads covalently coupled to its ligand. Which of the following is the most likely antibody preparation? A. Monoclonal anti-CD19 B. Monoclonal anti-CD56 C. Papain-treated anti-CD19 D. Papain-treated anti-CD56 E. Pepsin-treated anti-CD19 F. Pepsin-treated anti-CD56
D. Papain-treated anti-CD56
A 3-year-old boy is evaluated for a possible immunodeficiency. He has suffered repeated infections of mucosal-surface pathogens and has shown delayed development of protective responses to the standard childhood vaccination. Immuno-electrophoresis of his serum demonstrates the absence of a macroglobulin peak and his sputum is devoid of secretory IgA. Normal numbers of B cells bearing monomeric IgM are found by flow cytometry, and serum level of monomeric IgA, IgE, and each of the 4 subclasses of IgG are normal. Which of the following deficiencies could account for these findings? A. Absence of CD40 B. Absence of J chains C. Absence of IL-4 D. Absence of dendritic cells E. Absence of tissue macrophages
B. Absence of J chains
Toxoplasma gondii is an intracellular parasite that lives inside phagocytic and nonphagocytic cells by generating its own intracellular vesicle. This may allow it to avoid recognition and killing by CD8+ lymphocytes, which require the presentation of foreign peptides transported into the endoplasmic reticulum and loaded onto MHC molecules that have
A. a β2 domain instead of β2 macroglobulin
B. invariant chains
C. a peptide-binding groove
D. a single transmembrane domain
E. two similar chains
D. a single transmembrane domain
A patient is shown to a have a mutation in his BTK tyrosine kinase gene. Which of the following stages of lymphocyte differentiation is blocked in this patient?
A. Differentiation of mature B cells into plasma cells
B. Generation of memory cells
C. Differentiation of pre-BV cells into immature B cells
D. Negative selection of B cells in the bone marrow
E. Activation of mature B cells
E. Activation of mature B cells
A patients presents with recurrent bacterial infections and is found to have low serum levels of IgA and IgG, but elevated concentrations of serum IgM. Flow cytometry of his LN cells reveal an absence of immune cells expressing CD40L. In which immune cells this surface
marker is normally found?
A. B cells expressing membrane IgG
B. Activated CD4+ T helper cells
C. NK cells in the spleen
D. All lymphocytes in peripheral lymphoid tissues
E. CD19 B cells in the bone marrow
B. Activated CD4+ T helper cells
A 5-year-old boy has a history of recurrent pneumococcal pneumonia, Pneumocystis carinii pneumonia (PCP), and bacterial ear infections. His maternal uncle and an older brother experienced the same symptoms, but he has an older sister who is healthy. Laboratory studies indicate normal numbers of B cells and T cells, and the serum contains mostly IgM and very little IgG. Which of the following immune cell interactions does not function normally in this patient? A. Dendritic cell and CD4+T cell B. Dendritic cell and CD8+T cell C. B cell and CD4+T cell D. B cell and CD8+ T cell E. CD4+T cell and CD8+ T cell
C. B cell and CD4+T cell
A 40-year-old male patient has a genetic deficiency leading to the expression of nonfunctional CD40 ligand (CD40L). In addition to defects in humoral immunity, the patient showed an impaired cell-mediated immunity as evident by increased susceptibility to infections caused by intracellular pathogens. Which statement correctly describes CD40L-dependent mechanisms involved in cell-mediated immunity?
A. CD40L-dependent isotype switching is required to produce antibody isotypes that activate T cells.
B. CD40 ligand is required for killing of CD40-expressing infected cells by CTLs.
C. CD40 ligand is required for maturation of CD4+ T cells in the thymus.
D. CD40 ligand on T cells binds to CD40 on macrophages and enhances their phagocytic and Ag-presenting properties.
E. CD40 ligand on T cells binds to B7-1 and B7-2 on APCs, and this enhances the function of the APCs.
D. CD40 ligand on T cells binds to CD40 on macrophages and enhances their phagocytic and Ag-presenting properties.
Class I MHC-restricted T cells against tumor antigens can be found in patients with various types of cancer. Which mechanism correctly explains activation of naive CD8+ T cells specific for mutated self-antigens in tumors?
A. Malignant transformation of CD8+ T cells
B. Tumor secretion of T cell-activating cytokines
C. Cross reaction of microbe-specific CD8+ T cells with tumor antigens
D. Cross-presentation of tumor antigens by APCs
E. Antigenic modulation
D. Cross-presentation of tumor antigens by APCs
Which one of the following cell types would be most potent at activating naive T cells? A. Kupffer cells B. B cells C. Follicular dendritic cells D. Neutrophils E. Langerhans cells
E. Langerhans cells
Which one of the following descriptions of cytokine interleukin-2 is NOT true?
A. MHC-restricted T cells against tumor antigens can be found in patients with various
B. Expression of its gene requires multiple transcription factors, such as Fos, Jun, and NFAT.
C. It acts as an autocrine growth factor for T cells.
D. It binds to CD25 on the cell membrane of T cells.
E. It is only involved in the proliferation of helper T cells and not CTLs. It primes T cells to apoptosis.
E. It is only involved in the proliferation of helper T cells and not CTLs. It primes T cells to apoptosis.
CD8 is a protein that functions as a coreceptor for a subset of T cells and plays a significant role in all of the following EXCEPT:
A. Recognition of peptide antigen bound to class I MHC molecules
B. Maturation of MHC class I–restricted T cells
C. Infection of T cells by human immunodeficiency virus (HIV)
D. Signaling via Lck tyrosine kinase to initiate T cell activation
E. Strengthening the binding of T cells to antigen-presenting cells, albeit with low affinity
C. Infection of T cells by human immunodeficiency virus (HIV)
Both CD28 and CTLA-4 are receptors on T cells that are critical for regulating T cell activation. In which one of the following ways does CD28 differ from CTLA-4?
A. Only CD28 binds the costimulatory ligands B7-1 and B7-2 expressed on professional antigen-presenting cells.
B. CD28 counteracts positive, pro-proliferative T cell signals delivered by CTLA-4.
C. CD28 is constitutively expressed on naive T cells, whereas CTLA-4 is expressed on activated T cells.
D. CD28 binds its ligand with 10-fold greater affinity than does CTLA-4.
E. CD28 is important for delivering “signal 1” for T cell activation, whereas CTLA-4 is important for delivering “signal 2.”
C. CD28 is constitutively expressed on naive T cells, whereas CTLA-4 is expressed on activated T cells.
A 2-year-old boy suffers from recurrent bacterial infection of his ears, sinuses, lungs, and skin; laboratory studies indicate absence of sialylated Lewis X on his leukocytes. He is diagnosed with leukocyte adhesion deficiency type 2 (LAD-2). Which type of adhesive interaction required for leukocyte migration is defective in this boy?
A. E-selectin ligand binding to E-selectin
B. CD4 binding to class II MHC
C. VLA-4 binding to VCAM-1
D. Ig Fc receptor binding to Ig-coated cells
E. LFA-1 binding to ICAM-1
A. E-selectin ligand binding to E-selectin
Neonates, elderly persons, and otherwise immunocompromised patients are particularly susceptible to infections with Listeria monocytogenes. These patients typically have fever and chills, often progressing to hypotension and septic shock. In healthy individuals, however, intracellular microbes are usually effectively phagocytosed and killed by macrophages, which become activated via: A. CD40L-CD40 interactions between activated T helper cells and macrophages B. CD28-B7 interactions between activated T cells and macrophages C. Fas ligand–Fas interactions between activated cytotoxic T lymphocytes and macrophages D. TCR-MHC class II interactions between activated T helper cells and macrophages E. LFA-1–ICAM-1 interactions between activated T cells and macrophages
A. CD40L-CD40 interactions between activated T helper cells and macrophages