A viral infection activates cytotoxic T cells, and a
bacterial infection activates helper T cells. Once
these T cells begin performing their immune
functions, what are they called?
A. Memory cells
B. Anergic cells
C. Effector cells
D. Naive cells
C. Effector cells
A helper T-cell clone produces IL-4 and
IL-5 but not IFN-gamma or IL-17. What best explains this
finding?
A. Subset-restricted cytokine programs
B. Uniform
cytokine secretion
C. Antibody class deletion
D. TCR chain editing
A. Subset-restricted cytokine programs
Effector helper T cells are classically divided into which three
major cytokine-producing groups?
A. Treg, Th0, NKT
B. CTL,
NK, Th0
C. Th1, Treg, Th2
D. Th1, Th2, Th17
D. Th1, Th2, Th17
A cell samples microbial products, reads
local cytokine signals, and determines how helper T
cells should respond. Which cell is being described?
A. Basophil
B. Dendritic cell
C. Eosinophil
D.
Plasma cell
B. Dendritic cell
A dendritic cell detects both microbial motifs and local soluble
immune signals. Which two input systems is it integrating?
A.
MHC and TCRs
B. Fc and complement receptors
C. PRRs and
cytokine receptors
D. BCRs and integrins
C. PRRs and cytokine receptors
Skin cells near an infection release a
characteristic mixture of signals that helps
dendritic cells identify the attack location. What are these
signals?
A. Cytokines
B. Antibodies
C.
Selectins
D. Defensins
A. Cytokines
An activated dendritic cell instructs a helper T cell how to respond.
Which output best conveys this plan?
A. Antibody and
complement
B. Histamine and leukotrienes
C. Perforin and
granzyme
D. Co-stimulation and cytokines
D. Co-stimulation and cytokines
A dendritic cell leaves infected intestinal tissue and primes a
helper T cell. Its instructions mainly reflect what prior
information?
A. T-cell receptor affinity
B. Local tissue
immune signals
C. Bone marrow stromal signals
D. Plasma
antibody concentration
B. Local tissue immune signals
A patient with gram-negative sepsis has
macrophage activation after recognition of LPS.
Which receptor is most directly involved?
A. TLR4
B.
TLR2
C. TLR3
D. TLR9
A. TLR4
A dendritic cell detects molecules from
gram-positive bacteria. Which Toll-like receptor is
classically involved?
A. TLR9
B. TLR3
C. TLR4
D. TLR2
D. TLR2
During a viral infection, dendritic cells detect
double-stranded RNA produced during replication.
Which receptor recognizes it?
A. TLR4
B. TLR3
C.
TLR2
D. TLR9
B. TLR3
A dendritic cell detects unmethylated CpG
DNA during infection. Which receptor is most associated
with this pattern?
A. TLR2
B. TLR4
C. TLR9
D. TLR3
C. TLR9
Unmethylated CpG dinucleotides are detected by innate
immune cells. This pattern most strongly suggests which source?
A. Bacterial DNA
B. Viral envelope
C. Fungal capsule
D. Helminth cuticle
A. Bacterial DNA
A dendritic cell presents
antigen plus IL-12 to a virgin helper T cell. Which helper
subset is most likely induced?
A. Th17
B. Th2
C.
Th0
D. Th1
D. Th1
Which cytokine trio best matches the classical Th1 profile?
A.
IL-4, IL-5, IL-13
B. TNF, IFN-gamma, IL-2
C. IL-17, IL-21,
IL-23
D. TGF-beta, IL-6, IL-23
B. TNF, IFN-gamma, IL-2
A Th1 response helps activate macrophages and
natural killer cells early in infection. Which
cytokine performs this function?
A. IL-2
B.
IFN-gamma
C. TNF
D. IL-4
C. TNF
A macrophage has already been activated during
intracellular infection. Which Th1 cytokine
helps keep it activated?
A. IFN-gamma
B. IL-5
C. IL-13
D. IL-21
A. IFN-gamma
A patient needs B-cell class switching toward human
IgG3 during a Th1 response. Which cytokine provides this
influence?
A. IL-23
B. IL-4
C. TNF
D. IFN-gamma
D. IFN-gamma
A cytokine keeps NK cells “charged up” and
promotes proliferation of CTLs, NK cells, and Th1
cells. Which cytokine is this?
A. IL-17
B.
IL-13
C. IL-2
D. IL-10
C. IL-2
Tissue invasion by a parasite causes
activated dendritic cells to polarize helper T cells
toward which cytokine subset?
A. Th17
B.
Th2
C. Th1
D. Th0
B. Th2
Which cytokine trio best matches the Th2 subset?
A. IL-4, IL-5,
IL-13
B. TNF, IFN-gamma, IL-2
C. IL-17, IL-21, IL-23
D. IL-12, TGF-beta, IL-6
A. IL-4, IL-5, IL-13
A Th2 cytokine acts as a growth
factor for helper T cells already secreting
Th2 cytokines. Which cytokine is it?
A. IL-5
B.
IL-13
C. IL-21
D. IL-4
D. IL-4
A helminth-associated immune response promotes
B-cell class switching toward IgE. Which cytokine
most directly supports this?
A. IL-2
B. IL-4
C.
IL-17
D. IFN-gamma
B. IL-4
A mucosal immune response encourages B cells to produce IgA
antibodies. Which Th2 cytokine is responsible?
A.
IL-13
B. IL-21
C. IL-5
D. TNF
C. IL-5
During intestinal parasite defense,
goblet-cell mucus production increases. Which
cytokine best explains this effect?
A. IL-17
B.
IL-23
C. IFN-gamma
D. IL-13
D. IL-13
Fungi attack a mucosal barrier.
Activated dendritic cells produce TGF-beta plus IL-6.
Which helper subset is favored?
A. Th17
B. Th1
C.
Th2
D. Th0
A. Th17
Extracellular bacteria attack mucosal
tissue. Dendritic cells produce TGF-beta and
IL-23. Which helper program is promoted?
A. Th2
B. Th1
C. Th17
D. Treg
C. Th17
Which cytokine set best matches the Th17 subset in this
material?
A. IL-4, IL-5, IL-13
B. IL-17, IL-21,
IL-23
C. TNF, IFN-gamma, IL-2
D. IL-10, TGF-beta, IL-12
B. IL-17, IL-21, IL-23
A growth factor expands helper T cells
producing the Th17 cytokine subset. Which cytokine is
this?
A. IL-23
B. IL-21
C. TNF
D. IFN-gamma
A. IL-23
A mucosal fungal infection triggers recruitment of massive
numbers of neutrophils. Which cytokine is most
responsible?
A. IL-5
B. IL-4
C. IL-21
D. IL-17
D. IL-17
B cells guarding mucosal surfaces begin
producing IgG3 and IgA. Which Th17 cytokine caused this
shift?
A. IL-6
B. IL-12
C. IL-21
D. IL-4
C. IL-21
A dendritic cell tells a helper T cell where to
migrate but gives no clear effector
instructions. What subset results?
A. Th1
B.
Th0
C. Th2
D. Th17
B. Th0
A helper T cell retains the ability to produce a broad range
of cytokines after incomplete dendritic-cell
instruction. What is this called?
A. Th2
polarization
B. Th1 commitment
C. Th17 maturation
D.
Th0 subset
D. Th0 subset
A Th0 cell reaches infected tissue and encounters cytokines specific
to that site. What happens next?
A. It adopts a relevant
subset
B. It becomes permanently anergic
C. It deletes its
TCR
D. It stops cytokine secretion
A. It adopts a relevant subset
A researcher finds helper T cells that do not fit neatly into Th1,
Th2, or Th17 categories. What is the best interpretation?
A. All
T cells are mislabeled
B. Only CTLs make cytokines
C. The
paradigm has exceptions
D. Dendritic cells lack cytokines
C. The paradigm has exceptions
A dendritic cell’s plan for helper T-cell activation is based on
co-stimulatory and cytokine signals received from inflamed tissue.
What does this emphasize?
A. Random T-cell polarization
B.
Context-dependent immune planning
C. Antibody-independent class
switching
D. Cytokine-free T-cell activation
B. Context-dependent immune planning
A Th1-polarized response becomes dominant during
infection. Which cytokine helps suppress proliferation of
competing Th2 cells?
A. IL-10
B. IFN-gamma
C. IL-5
D. IL-13
B. IFN-gamma
A Th2 response is limiting excessive Th1
expansion. Which cytokine most directly mediates this
inhibition?
A. IFN-gamma
B. IL-2
C. IL-17
D. IL-10
D. IL-10
A patient mounts a strong Th1 response against an intracellular
pathogen. Which competing helper subset is directly suppressed
by IFN-gamma?
A. Th2
B. Th17
C. Th0
D. Treg
A. Th2
A patient with helminth infection develops a strong Th2 response.
IL-10 from these cells decreases proliferation of
which subset?
A. Th0
B. Th17
C. Th1
D. CTL
C. Th1
Why do Th helper subsets inhibit one another?
A. To increase
antibody diversity
B. To prevent competing activation
C.
To destroy infected cells
D. To increase cytokine range
B. To prevent competing activation
What is a cytokine property?
A. Limited local range
B.
Permanent receptor binding
C. Systemic endocrine spread
D.
Antigen-specific recognition
A. Limited local range
A student assumes cytokines behave mainly like hormones traveling
throughout the body. Which correction is best?
A. They mostly
enter lymphatics
B. They mostly activate platelets
C. They
mostly bind antibodies
D. They mostly act locally
D. They mostly act locally
A patient receives intradermal tuberculin and
returns days later for evaluation. What immune phenomenon is being
tested?
A. Type I hypersensitivity
B. Immune-complex
disease
C. Delayed-type hypersensitivity
D.
Complement-mediated lysis
C. Delayed-type hypersensitivity
The tuberculosis skin test requires waiting several days after
tuberculin injection. This delay best reflects which process?
A.
T cell-mediated inflammation
B. Immediate mast-cell
degranulation
C. IgE-mediated wheal formation
D. Direct
bacterial toxin injury
A. T cell-mediated inflammation
A cytotoxic T lymphocyte kills a virus-infected epithelial
cell by delivering enzymes into the target
cell. Which pair is most involved?
A. FasL and
IL-10
B. Perforin and granzyme B
C. IFN-gamma and
IL-4
D. IL-17 and IL-23
B. Perforin and granzyme B
A CTL releases a molecule that disrupts the target cell
membrane, allowing entry of apoptotic
enzymes. Which molecule does this?
A. Granzyme B
B. IFN-gamma
C. IL-10
D. Perforin
D. Perforin
A CTL delivers an enzyme into an infected target cell,
triggering apoptosis. Which molecule is responsible?
A. Perforin
B. FasL
C. Granzyme B
D. IL-2
C. Granzyme B
A cytotoxic T cell uses a death-receptor pathway
instead of granule exocytosis. Which molecule on the
CTL is responsible?
A. Fas ligand
B. Granzyme B
C.
IFN-gamma
D. IL-17
A. Fas ligand
Fas ligand on a CTL triggers apoptosis by binding which target-cell
structure?
A. Class I MHC
B. TLR4
C. CD28
D.
Fas receptor
D. Fas receptor
A CTL secretes IFN-gamma near infected cells. What
is the main local effect?
A. Decrease class II MHC
B.
Increase class I MHC
C. Suppress Fas expression
D. Block
granzyme uptake
B. Increase class I MHC
Why does CTL-derived IFN-gamma help future CTL
recognition?
A. It increases IgE switching
B. It recruits
eosinophils locally
C. It raises MHC I expression
D. It
suppresses viral apoptosis
C. It raises MHC I expression
A virus-infected cell is killed by apoptosis rather than necrosis.
Why is apoptosis safer locally?
A. Less surrounding tissue
damage
B. More enzyme leakage occurs
C. More complement
activation occurs
D. Greater neutrophil rupture occurs
A. Less surrounding tissue damage
Necrosis of an infected cell can worsen nearby injury because it
releases which contents?
A. Antibodies and cytokines
B.
MHC and TCRs
C. Enzymes and chemicals
D. Perforin and FasL
C. Enzymes and chemicals
A CTL induces apoptosis in a virus-infected cell before viral
assembly is complete. What benefit does this provide?
A. Preserves viral RNA
B. Destroys viral nucleic acids
C.
Blocks MHC I expression
D. Activates bacterial CpG DNA
B. Destroys viral nucleic acids
Why is apoptosis especially useful in virus-infected cells?
A.
It causes tissue swelling
B. It releases lysosomal enzymes
C. It promotes immediate necrosis
D. It destroys viral DNA/RNA
D. It destroys viral DNA/RNA
A cytotoxic T cell uses three major weapons against infected host
cells. Which set is most complete?
A. IL-4, IL-5, IL-13
B.
TLR2, TLR3, TLR9
C. Perforin, FasL, IFN-gamma
D. IgA, IgE, IgG3
C. Perforin, FasL, IFN-gamma
A patient has a positive tuberculosis skin test. Which statement best
describes the test?
A. Tuberculin causes immediate IgE
release
B. Tuberculin triggers delayed hypersensitivity
C.
Tuberculin directly lyses macrophages
D. Tuberculin detects
serum antibodies
B. Tuberculin triggers delayed hypersensitivity