Which statement best defines hypersensitivity?
A. A normal immune response that clears infection without
damage
B. A genetic defect in immune cell development
C.
An exaggerated or inappropriate immune response that causes tissue
damage
D. A response limited only to autoimmune diseases
C. An exaggerated or inappropriate immune response that causes tissue damage
Which type of immunity primarily functions against parasitic
infections?
A. Type 1
B. Type 2
C. Type 3
D.
Type 4
B. Type 2
Which of the following is not a characteristic of
parasites?
A. Large multicellular organisms
B. Easily
phagocytosed
C. Complex eukaryotic structure
D. Evasive
immune strategies
B. Easily phagocytosed
What is the body’s general immune strategy for eliminating parasites?
A. Type 1 immunity involving neutrophils and IFN-γ
B. Type 2
immunity using IgE, mast cells, and eosinophils to promote expulsion
via mucus, coughing, and peristalsis
C. Type 3 immunity using
complement activation only
D. Cytotoxic T-cell–mediated killing
through perforin and granzyme
B. Type 2 immunity using IgE, mast cells, and eosinophils to promote expulsion via mucus, coughing, and peristalsis
Which cytokines are key mediators of Type 2 immunity?
A. IL-2,
IFN-γ, TNF
B. IL-4, IL-5, IL-13
C. IL-6, IL-8, IL-12
D. IL-10, IL-17, IL-23
B. IL-4, IL-5, IL-13
Why is switching from IgE to IgG important during allergic responses?
A. IgG4 enhances mast cell activation and increases histamine
release
B. IgG4 blocks allergens from binding IgE, reducing mast
cell activation and chronic inflammation
C. IgG4 increases
eosinophil degranulation, worsening allergic symptoms
D. IgG4
promotes complement activation to intensify inflammation
B. IgG4 blocks allergens from binding IgE, reducing mast cell activation and chronic inflammation
Which antibody binds most tightly to FcεRI receptors on mast
cells?
A. IgA
B. IgE
C. IgG4
D. IgM
B. IgE
What is Ozalimumab, and how does it work?
A. A monoclonal antibody that blocks IL-5 to prevent eosinophil
activation
B. A monoclonal antibody that binds free IgE,
reducing mast-cell activation and slightly increasing infection
risk
C. A drug that destroys mast cells directly to reduce
allergic reactions
D. A vaccine that induces tolerance to food allergens
B. A monoclonal antibody that binds free IgE, reducing mast-cell activation and slightly increasing infection risk
Which of the following cells release major basic protein to kill
parasites?
A. Mast cells
B. Basophils
C.
Eosinophils
D. Dendritic cells
C. Eosinophils
How do mast cells contribute to defense against parasites?
A. They phagocytose parasites directly and digest them with
lysosomal enzymes
B. They produce IgM to neutralize parasites in
the bloodstream
C. They reside in tissues and, when IgE is
cross-linked, degranulate to release histamine and proteases that
drive inflammation and parasite expulsion
D. They activate
complement to kill parasites intracellularly
C. They reside in tissues and, when IgE is cross-linked, degranulate to release histamine and proteases that drive inflammation and parasite expulsion
Which histamine receptor is primarily responsible for inflammation
and smooth muscle contraction?
A. H1
B. H2
C.
H3
D. H4
A. H1
What are secondary mediators, and how does aspirin affect them?
A. Protein cytokines released before degranulation; aspirin
increases their production
B. Lipid mediators such as
prostaglandins and leukotrienes made after degranulation; aspirin
blocks COX enzymes to reduce prostaglandin synthesis
C.
Antibodies produced by plasma cells; aspirin prevents class
switching
D. Histamine molecules stored in granules; aspirin
neutralizes them directly
B. Lipid mediators such as prostaglandins and leukotrienes made after degranulation; aspirin blocks COX enzymes to reduce prostaglandin synthesis
What type of molecule is most likely to act as an allergen?
A.
Large insoluble protein
B. Small soluble protein structurally
similar to parasite antigen
C. Nucleic acid fragment
D.
Lipid antigen
B. Small soluble protein structurally similar to parasite antigen
Which best describes the process of sensitization in allergic responses?
A. Immediate mast cell degranulation upon first allergen
exposure
B. Initial exposure to allergen leads to Th2
differentiation, B-cell class switching to IgE, and IgE binding to
mast cells, priming them for future exposures
C. IgG production
that blocks allergen binding to mast cells
D. Activation of
cytotoxic T cells that directly kill allergen-expressing cells
B. Initial exposure to allergen leads to Th2 differentiation, B-cell class switching to IgE, and IgE binding to mast cells, priming them for future exposures
Which environmental factor decreases allergy risk?
A.
Antibiotic use
B. Excessive hygiene
C. Early parasite
exposure
D. Urban pollution
C. Early parasite exposure
Which of the following genes or proteins, when altered, can affect allergy susceptibility?
A. IL-4R, STAT6, Filaggrin
B. HLA, FCER1A, IL-4R
C.
STAT6, FCER1A, Filaggrin
D. All of the above
D. All of the above
The “wheal and flare” reaction in skin testing is caused by:
A.
Complement activation
B. Mast cell degranulation
C.
Cytotoxic T cells
D. Neutrophil infiltration
B. Mast cell degranulation
Which best differentiates the early and late phases of an allergic response?
A. Early phase occurs hours later via cytokines; Late phase occurs
within minutes via histamine
B. Early phase = histamine release
within minutes; Late phase = cytokine-mediated inflammation hours
later
C. Both early and late phases are mediated only by
IgG
D. Early phase involves antibody production; Late phase
involves mast cell degranulation
B. Early phase = histamine release within minutes; Late phase = cytokine-mediated inflammation hours later
A patient eats peanuts and experiences hypotension, airway constriction, and swelling. What type of hypersensitivity is this?
A. Type II
B. Type I
C. Type III
D. Type IV
B. Type I treated with epinephrine
Which of the following is not a symptom of allergic
asthma?
A. Airway constriction
B. Mucus production
C. IL-13 activity
D. Complement deposition
D. Complement deposition
How does desensitization (allergen immunotherapy) work?
A. Gradual allergen exposure increases IgE and mast cell
activation
B. Rapid allergen exposure triggers immediate
tolerance via T-cell deletion
C. Gradual allergen exposure
increases IgG4 and reduces IgE, promoting immune tolerance
D.
Allergen exposure only stimulates innate immunity without affecting antibodies
C. Gradual allergen exposure increases IgG4 and reduces IgE, promoting immune tolerance
Type II hypersensitivity is primarily mediated by:
A. T
cells
B. IgE
C. IgG or IgM
D. Immune complexes
C. IgG or IgM
A newborn develops anemia due to maternal antibodies crossing the placenta. What is this condition?
A. Hemophilia
B. Erythroblastosis fetalis
C.
Thalassemia
D. Sickle cell anemia
B. Erythroblastosis fetalis, TYPE II
Which mechanism mediates Type III hypersensitivity?
A.
Antibody-dependent cellular cytotoxicity
B. Immune complex
deposition
C. Mast cell degranulation
D. Delayed T cell response
B. Immune complex deposition
What is serum sickness?
A. A Type I hypersensitivity reaction to food allergens
B. A
Type II reaction causing hemolysis
C. A Type III
hypersensitivity reaction caused by immune complex deposition after
exposure to foreign serum
D. A Type IV T-cell–mediated delayed reaction
C. A Type III hypersensitivity reaction caused by immune complex deposition after exposure to foreign serum
Which of the following are common symptoms of serum sickness?
A. Vasculitis, arthritis, and nephritis
B. Anaphylaxis,
hypotension, and airway constriction
C. Fever only
D. Skin
rash without systemic involvement
A. Vasculitis, arthritis, and nephritis
Which of the following is not associated with Type
IV hypersensitivity?
A. Tuberculin skin test
B. Contact
dermatitis
C. Serum sickness
D. Poison ivy rash
C. Serum sickness
Which best describes the difference between the sensitization and effector phases of delayed-type hypersensitivity (DTH)?
A. Sensitization = immediate mast cell degranulation; Effector =
antibody production
B. Sensitization = memory Th1 cells form;
Effector = re-exposure triggers cytokine release and macrophage
recruitment
C. Sensitization = IgE production; Effector =
eosinophil-mediated cytotoxicity
D. Sensitization and effector
phases are identical
B. Sensitization = memory Th1 cells form; Effector = re-exposure triggers cytokine release and macrophage recruitment
Which statement best defines chronic inflammation and explains why it is problematic?
A. Short-term immune response that eliminates pathogens without
tissue damage
B. Persistent immune activation causing tissue
damage, fibrosis, and potential organ failure
C. Inflammation
limited to the skin and mucosa only
D. A beneficial process that
always improves tissue repair
B. Persistent immune activation causing tissue damage, fibrosis, and potential organ failure