Clinical Immunology
Chapter Exam Questions
Course Introduction
Clinical Immunology explores the mechanisms of the immune system with a focus on their relevance to human health and disease. The course examines immune responses in the context of infection, autoimmunity, allergy, transplantation, immunodeficiency, and cancer, emphasizing both diagnostic and therapeutic applications in clinical practice. Through an integration of foundational immunological concepts with case-based discussions, students gain a comprehensive understanding of how immune dysfunction contributes to various clinical disorders and how these insights guide modern medical interventions.
Recommended Textbook
Immunology for Pharmacy 1st Edition by Dennis Flaherty PhD
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Page 2
Chapter 1: Cells and Organs of the Immune System
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Q1) Hematopoiesis is the:
A) Development of blood cells
B) Development of cancer cells
C) Development of immune cells
D) Development of immune response
Answer: A
Q2) As a result of leukocyte adhesion deficiency, white blood cells cannot:
A) Present antigen
B) Release granules
C) Perform diapedesis
D) Phagocytose pathogens
Answer: C
Q3) Monocytes are primarily located in the:
A) Liver
B) Blood
C) Spleen
D) Lymph nodes
Answer: B
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3
Chapter 2: Innate Immunity
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Q1) Cathelicidins perform which of the following functions?
I. Chemotaxis
II. Neutralization of endotoxins
III. Broad spectrum antimicrobial activity
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Answer: E
Q2) Activation of a phagocyte by Toll-like receptors (TLRs) bound to a pathogen triggers what innate immune response?
A) Phagocytosis
B) Complement activation
C) Cathelicidin production
D) Decrease in body temperature
Answer: A
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Chapter 3: Immunogenicity and Antigenicity
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Q1) RhoGAM administered to an Rh-negative mother would help the patient by:
I- Preventing production of anti-Rh antibodies
II- Preventing fetal hemolysis in future pregnancies
III- Preventing transfusion reactions due to ABO mismatch
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Answer: C
Q2) When a low molecular weight (<3000 Da) pharmaceutical agent binds to albumin, the pharmaceutical agent is acting as a/an:
A) Hapten
B) Allergen
C) Immunogen
D) Carrier protein
Answer: A
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Page 5
Chapter 4: Antigen Presenting Molecules
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Q1) Human leukocyte antigen (HLA) class I molecules bind antigens:
A) At the ends and the antigens are larger than HLA class II antigens
B) At the ends and the antigens are smaller than HLA class II antigens
C) In the middle and the antigens are larger than HLA class II antigens
D) In the middle and the antigens are smaller than HLA class II antigens
Q2) HLA class III genes produce:
A) Stress molecules
B) Complement components
C) Antigen presenting molecules
D) Receptors that activate natural killer (NK) cells
Q3) Individuals who express HLA-DR13:
A) Can more easily clear hepatitis B virus
B) Are more susceptible to tuberculosis infection
C) Are more susceptible to Candida albicans infections
D) Can more easily eliminate respiratory syncytial virus (RSV)
Q4) A set of HLA antigens on the same chromosome is called a:
A) Gene
B) Hapten
C) Haplotype
D) Single nucleotide polymorphism (SNP)
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Chapter 5: Antigen Presenting Cells
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Q1) Kupffer cells are a type of macrophage located in the:
A) Liver
B) Bone
C) Brain
D) Connective tissue
Q2) Dendritic cells are important parts of the immune response because they are:
A) Able to produce antibody
B) Circulating in the blood waiting for antigen
C) Able to kill tumor cells and virally-infected cells
D) Located in areas that are likely sites of pathogen entry
Q3) Which type of dendritic cell does not present antigen, but instead aids B cell maturation into plasma cells?
A) Langerhans cells
B) Follicular dendritic cells
C) Interstitial dendritic cells
D) Plasmacytoid dendritic cells
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Chapter 6: Surface Interactions Between T Cells and
Antigen-Presenting Cells
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Q1) The interaction between CTLA-4 and B7 leads to:
A) Downregulation of T cell signaling
B) Stabilization of the TCR/APC interaction
C) B cell activation and generation of memory cells
D) Production of proteins that regulate the cellular response to interleukin-2 (IL-2)
Q2) CD4 molecules on T cells bind to:
A) CD40
B) B7 molecules
C) MHC class I molecules
D) MHC class II molecules
Q3) In the function of the TCR, the purpose of the CD3 complex is to:
A) Bind antigen
B) Transduce signals
C) Anchor the TCR in the membrane
D) Stabilize the interaction between the TCR and the APC
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8
Chapter 7: Intracellular Signaling and T Cell Activation
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Q1) Which of the following is an example of autocrine signaling?
A) An NK cell responding to IL-12 produced by a macrophage.
B) A macrophage responding to TNF made by the same macrophage.
C) A T helper cell responding to IL-2 produced by a neighboring T cell.
D) A neutrophil responding to IL-1 produced by vascular endothelial cell.
Q2) Which of the following is/are part of the high affinity IL-2 receptor?
I. a-Chains
II. b-Chains
III. g-Chains
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Q3) The major defect in X-linked severe combined immunodeficiency (SCID) is:
A) Inability to produce IL-2
B) Lack of ZAP-70 protein kinase
C) Inability to produce B or T cells
D) Lack of g-chain in interleukin receptors
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Page 9
Chapter 8: B Cell Activation and Signaling
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Q1) Which of the following is an example of a type I thymus-independent antigen?
A) Bacterial enzyme
B) Viral protein coat
C) Lipopolysaccharide (LPS)
D) Pneumococcal capsular polysaccharide
Q2) Long-lived plasma cells are most likely to be produced in response to:
A) Thymic-dependent antigens
B) Type I thymic-independent antigens
C) Type II thymic-independent antigens
D) Both thymic-dependent and thymic-independent antigens result in production of long-lived plasma cells
Q3) X-linked agammaglobulinemia results from a defect in:
A) IL-7 gene
B) BTK gene
C) BLyS gene
D) CD22 gene
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Chapter 9: Antibodies
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Q1) Which region of the antibody is important for physical flexibility of the antigen binding region?
A) J chain
B) Hinge region
C) Secretory piece
D) Variable regions
Q2) Which class of antibody causes the release of histamine-containing granules of basophils and mast cells?
A) IgA
B) IgE
C) IgG
D) IgM
Q3) During the anamnestic response, IgM-producing plasma cells switch to producing which type of antibody?
A) IgA
B) IgD
C) IgE
D) IgG
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11
Chapter 10: Antibody Diversity
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Q1) The addition of N-nucleotides has which effect on antibody structure?
A) Determines if the light chain is a l-chain or k-chain
B) Allows for removal of amino acids in the open hairpins
C) Adds the C4 region to the heavy chain of some antibodies
D) Changes the amino acid sequence in the hypervariable CDR3
Q2) What is the purpose of the recognition signal sequences (RSSs) in rearrangement of genes?
A) The RSSs are the coding regions of the DNA.
B) The RSSs are the enzymes that facilitate recombination.
C) The RSSs are spacers that align genes on the same side of DNA.
D) The RSSs are the areas that determine the antigen-binding pocket.
Q3) During recombination, which enzymes are responsible for formation of the DNA hairpins?
A) Endonucleases
B) RAG1 and RAG2
C) Artemis and DNA-dependent kinase (DNA-PK)
D) Multiple terminal deoxynucleotidyl transferases
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Page 12
Chapter 11: Complement
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Q1) In the alternative pathway, C3b can bind to which of the following?
I. To C3bBb
II. To factor B
III. The microbe cell surface
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Q2) The role that C3d plays in the immune response to pathogens is:
A) Activation of B cells
B) Activation of CD4 and CD8 T cells
C) Activation of the alternative pathway
D) Activation of inhibitory factors of the complement pathways
Q3) Which of the following complement components acts as a chemoattractant?
A) C2a
B) C3a
C) C4b
D) C5b
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Page 13
Chapter 12: Phagocytosis and Intracellular Killing
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Q1) What is the purpose of complement receptor binding to complement fragments during phagocytosis?
A) Reduces production of ATP
B) Causes production of catalase
C) Triggers production of superoxide
D) Facilitates internalization of pathogen
Q2) Following phagocytic ingestion of a pathogen, which of the following occurs?
A) Pinocytosis
B) Phagosome fusion with granules
C) Binding to antibody by Fc receptor on phagocyte
D) Binding to complement fragments by complement receptors
Q3) Which is a key component in oxygen-independent phagocytic killing?
A) Lysozyme
B) Myeloperoxidase
C) Hypochlorous acid
D) Superoxide dismutase
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14
Chapter 13: Antibodies and in Vivo Therapy
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Q1) Radiolabeled antibodies to CD20, including tositumomab labeled with iodine-131, are frequently used to treat which disorder?
A) Multiple myeloma
B) Rheumatoid arthritis
C) Non-Hodgkin's lymphoma
D) Human immunodeficiency virus (HIV)
Q2) Hybridomas are fusion cells composed of:
A) B cells and T cells
B) Two different myeloma cells
C) Splenic B cells and myeloma cells
D) Lymph node B cells and splenic B cells
Q3) Which of the following is an example of active immunity?
A) Antibody used therapeutically to treat lymphoma
B) Immunity to pneumococcal infection after exposure to the organism
C) Immunity acquired in a child by passage of antibodies from the mother's milk
D) Administration of pooled immunoglobulins from patients that had recovered from cytomegalovirus (CMV) to patients that currently have the disease
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15
Chapter 14: Antibodies and in Vitro Research and Diagnostic Assays
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Q1) In flow cytometry, side scatter is a measure of:
A) Cell size
B) Protein content
C) Granularity of a cell
D) Expression of CD markers
Q2) To identify different surface markers on a population of cells, flow cytometry requires the use of:
A) Enzymes
B) Colorimetric dyes
C) Radioactive isotopes
D) Fluorescent antibodies
Q3) Which test is used to confirm a diagnosis of HIV-positive after initial testing?
A) Flow cytometry
B) Western blotting
C) Immunochromatographic assay
D) Enzyme-linked immunosorbent assay
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Chapter 15: Immediate Allergic Reactions
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Q1) Which of the following is/are responsible for class switching to IgE production in allergic reactions?
I. IL-5
II. IL-4
III. IL-13
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Q2) Oral allergy syndrome is caused by:
A) Food allergies
B) Overproduction of eosinophils
C) Bacterial infection that stimulates IgE production
D) Cross reaction between shared antigens on food and pollen
Q3) What role does histamine play in allergic reactions?
A) Increases vascular permeability
B) Stimulates eosinophil production
C) Stimulates granule release from mast cells
D) Prevents activation of the coagulation cascade
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Chapter 16: Autoimmunity
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Q1) Cytomegalovirus (CMV), as well as other infections, may contribute to the development of which autoimmune disorder?
A) Diabetes
B) Myasthenia gravis
C) Pernicious anemia
D) Systemic lupus erythematosus (SLE)
Q2) What is the function of thyroid stimulating hormone (TSH)?
A) Stimulates production of TSH
B) Stimulates production of thyroglobulin
C) Stimulates production of thyroid releasing hormone (TRH)
D) Stimulates production of triiodothyronine (T ) and thyroxine (T )
Q3) Most patients with Hashimoto's thyroiditis have antibodies to:
A) T and T
B) Thyroglobulin
C) TSH receptors
D) TRH receptors
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18
Chapter 17: Transplantation
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Q1) How is the T cell response during transplant rejection different from the response during an infection?
A) Few T cells are responding during rejection
B) No T cells respond during rejection, only B cells
C) The number of T cells responding is much higher during rejection
D) The same amount of cells respond, but the response is stronger during rejection
Q2) Direct antigen presentation occurring during allogeneic graft rejection occurs when:
A) Donor APCs present antigen to the donor T cells
B) A recipient's T cells recognize donor cells as foreign
C) Donor antibodies bind to recipient cell surface molecules
D) A recipient's T cells recognize foreign antigen processed on the recipient's APCs
Q3) Without genetic modification, what is the main cause of rejection in xenotransplants?
A) Transfer of infection
B) Organs are the wrong size
C) The minor HLA antigens do not match
D) Pre-existing antibodies to alpha-galactosyl
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19
Chapter 18: Antigen Presentation for Cell-Mediated Response
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Q1) What is the purpose of b -microglobulin associated with MHC class I molecules?
A) Stabilization
B) Interacts with T cell
C) Anchors to membrane
D) Scaffolding molecule between TAP and MHC class I molecule
Q2) As antigen is processed prior to loading onto MHC class I molecules, the antigens are degraded into smaller fragments by the:
A) Proteasome
B) Golgi apparatus
C) Phagolysosome
D) Endoplasmic reticulum (ER)
Q3) MHC class I molecules present antigen to:
A) NK cells
B) CD8 T cells
C) CD4 Th1 cells
D) CD4 Th2 cells
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Page 20
Chapter 19: Delayed Type Hypersensitivity Reactions
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Q1) Which of the following can be found inside a granuloma?
A) Basophils
B) Eosinophils
C) Neutrophils
D) Macrophages
Q2) Which of the following is present in bat droppings, putting cavers at risk for this disease?
A) Coccidioides immitis
B) Histoplasma capsulatum
C) Mycobacterium tuberculosis
D) Mycobacterium avium complex (MAC)
Q3) In which stage of TB infection does lung necrosis caused by macrophage-derived reactive oxygen species (ROS) begin?
A) The first phase
B) The second phase
C) The third phase
D) The final phase
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21
Chapter 20: Cytotoxic T Cells
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Q1) The main immunological defect in familial erythrophagocytic lymphohistiocytosis type 2 is:
A) Inability to synthesize perforin
B) Production of nonfunctional granzymes
C) Inability to secrete perforin and granzymes
D) Production of reduced amounts of cathepsin C
Q2) What role does perforin perform in the death of target cells?
A) Perforin activates caspases.
B) Perforin creates a pore in the host cell.
C) Perforin disrupts mitochondrial function.
D) Perforin cleaves and activates granzymes.
Q3) Tumor infiltrating lymphocytes (TILs) found in a solid tumor or melanoma may indicate:
A) A good prognosis due to small tumor size
B) A bad prognosis due to an aggressive cancer
C) A good prognosis due to a vigorous immune response
D) A bad prognosis due to damage to surrounding tissue by the immune system
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Chapter 21: Natural Killer Cells
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Q1) Individuals with Chediak-Higashi syndrome have a genetic defect that causes:
A) The increased production of IL-13
B) Increased numbers of NKT type I cells
C) The inability to kill through the perforin and granzymes pathway
D) The inability to produce activating and inhibiting receptors in the NK cell surface
Q2) NKT cells require antigen presentation by:
I- CD1
II- MHC class I molecules
III- MHC class II molecules
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Q3) Which of the following is true concerning natural killer (NK) cells?
A) NK cells never express CD16.
B) NK cells never express CD56.
C) NK cells express both B and T cell markers.
D) NK cells do not express B or T cell markers.
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Page 23
Chapter 22: Factors That Influence the Immune Response
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Q1) Which methods of antigen administration elicit a vigorous immune response?
I. Intravenous
II. Intramuscular
III. Subcutaneous
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
Q2) Antigen-induced cell death (AICD) is mediated by:
I- Fas:FasL interactions
II- Perforin and granzymes
III- TNF-mediated cell death
A) I only
B) III only
C) I and II
D) II and III
E) I, II, and III
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Chapter 23: Cytokines and Biological Modifiers
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Q1) Which of the following is a marker for melanoma?
A) AFP
B) CEA
C) MART-1
D) Sialyl Tn antigen
Q2) What is the mechanism of action of the sipuleucel-T prostate cancer vaccine?
A) Dendritic cells are incubated with a fusion protein containing prostate specific antigen (PSA) and GM-CSF.
B) A plasmid that codes for an antibody that expresses prostate specific antigen (PSA), and dendritic cells present PSA to T cells.
C) A single B cell clone that is tumor specific is grown in the lab and infused into the patient to produce large amounts of tumor specific antibody.
D) Patient tumor cells are exposed to a viral vector containing a gene for prostate specific antigen (PSA), and then the tumor cells are infused into the patient to stimulate an immune response.
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Chapter 24: Vaccines in Theory and Practice
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Q1) Why are toxoid vaccines an effective means for reducing bacterial illness?
A) The toxin causes the damage, not the bacteria.
B) Bacteria have to die before the toxins can cause damage.
C) The toxins stimulate the immune system better than bacteria.
D) Bacteria have the toxins on their surface, so an immune response to the toxins will neutralize both.
Q2) Why do adenovirus vaccine vectors have limited utility?
A) Adenoviruses are small and cannot incorporate large numbers of genes from other viruses.
B) Most humans have preexisting antibodies that neutralize the vector before it can reach target tissue.
C) The immune response is weaker because the vector displays antigens from both the adenovirus and the pathogenic virus, diluting the immune response.
D) If the adenovirus incorporates large numbers of genes from pathogenic viruses, it may lose the ability to infect host tissue and elicit an immune response.
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Chapter 25: Vaccine-Preventable Diseases
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Q1) Why will the Zostavax vaccine be phased out over time?
A) Because the virus can mutate and the vaccine will no longer be effective
B) Because with prolonged use of the vaccine, patients will no longer mount a proper immune response to the virus
C) Because older patients are less likely to be able to afford the vaccine, so it is more cost effective to vaccinate children
D) Because all children will have been vaccinated against Varicella zoster so they will not get shingles when they are older
Q2) What is the main symptom of rotavirus infection?
A) Cough
B) Diarrhea
C) Cold sore
D) Swollen salivary glands
Q3) Corynebacterium diphtheriae colonizes:
A) Heart and liver
B) Muscle and liver
C) Tonsils and pharynx
D) Kidneys and adrenal glands
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Chapter 26: Acquired Immune Deficiency Syndrome
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Q1) What protein protects viral RNA from degradation by host cell cytoplasmic enzymes?
A) gp120
B) RNase
C) Vif protein
D) Rev protein
Q2) During the initial infection with HIV, the virus is concentrated in the:
A) Thymus
B) Bone marrow
C) Lymph nodes
D) Site of exposure
Q3) The most important enzyme involved in transcription of HIV RNA into DNA is:
A) Integrase
B) RNA polymerase
C) Late phase protease
D) Reverse transcriptase
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