WorksheetsAllergies: Initial & Subsequent Exposure
Total questions: 83
Worksheet time: 42mins
In the diagram, what is the primary function of IgE produced after initial allergen exposure?
Drives T cell cytotoxic killing of allergens
Neutralizes circulating pathogens broadly
Tags allergen for mast cell sensitization
Blocks allergen from binding epithelial cells
Which sequence correctly orders events from first exposure to allergic reaction in the diagram?
Allergen binds mast cell, B cell forms IgG, histamine releases
B cell activation, plasma cell makes IgE, mast cell sensitization
IgE binds allergen in blood, mast cell creates antibodies
Mast cell degranulation, allergen entry, B cell activation
During subsequent exposure, which mechanism leads directly to symptom onset?
Eosinophil phagocytosis of allergens
Complement cascade lyses mast cells
T cell receptor engagement induces apoptosis
Cross-linking of IgE triggers mast cell degranulation
Which cells are explicitly depicted as producing IgE in the initial exposure sequence?
Naive B cells
Plasma cells
Mast cells
Epithelial cells
Select all statements that are supported by the diagram.
Histamine release follows allergen-induced IgE cross-linking
B cells directly degranulate to release histamine
IgE production occurs only after subsequent exposure
Mast cells express IgE receptors before allergen exposure
Which shared immune feature best links responses to allergens and helminth parasites under the hygiene hypothesis?
Dominant TH1 macrophage activation with strong IFN-γ
Bias toward TH2 cytokine polarization and IgE production
Robust cytotoxic CD8 responses with perforin release
Exclusive mucosal IgA without eosinophil recruitment
During a primary response to a novel allergen, which sequence most accurately describes early events leading to immune cell arming?
Naive B cells secrete IgA first, basophils bind via FcαRI
TH1 priming, class switch to IgG3, NK cell arming via FcγRIII
Direct B cell activation to IgG1, complement fixation on mast cells
Antigen presentation to TH2, IL-4 driven class switch to IgE, FcεRI loading
Which cells are principal effectors in the TH2-driven secondary response against parasites and allergens?
Basophils producing IL-4 and IL-13
Eosinophils with cytotoxic granule release
Cytotoxic CD8 T lymphocytes
Mast cells with rapid degranulation
Neutrophils mediating NET formation
Identify the typical order of antibody isotypes during class switching in a secondary response to allergens or parasites.
Initial IgM then switch to IgG then IgE
Initial IgM then switch to IgE then IgG
Initial IgA then switch to IgM then IgE
Initial IgD then switch to IgM then IgG
Match each hypersensitivity type with its defining mechanism.
Type IV involves delayed T cell–mediated inflammation
Type IV involves immediate complement-driven cytolysis
Type III involves immune complex deposition and inflammation
Type II involves antibodies targeting cell surface antigens
Type I involves IgE-mediated mast cell degranulation
Why is intramuscular epinephrine first-line treatment for anaphylaxis?
It neutralizes IgE antibodies directly in blood
It induces durable desensitization of mast cells
It reverses airway edema and vasodilation rapidly
It blocks complement activation at C3 convertase
Which pairing correctly links an allergy test or treatment with its immune mechanism?
Omalizumab binds FcεRI to block mast cell activation
Antihistamines prevent eosinophil granule protein release
Allergen immunotherapy skews immunity away from TH2 bias
Serum specific IgE assesses allergen-specific sensitization
Skin prick test detects immediate IgE-mediated reactivity
Which statement best distinguishes self-antigens from non-self antigens in immune function?
Non-self antigens are host molecules causing autoimmunity
Self-antigens are pathogens always targeted for killing
Non-self antigens are harmless molecules always ignored
Self-antigens are host molecules tolerated by immunity
Harmless antigens that can still trigger an immune response are called what?
Immunogens
Autoantigens
Adjuvants
Allergens
Which scenario exemplifies a hypersensitivity reaction?
No reaction after seasonal pollen exposure
Sneezing after repeated exposure to cat dander
Fever from first-time influenza infection
Tolerance to commensal gut microbiota
During initial exposure to an allergen, what key immunological event sets up future reactions?
Generation of memory cells specific to the allergen
Massive histamine release from mast cells
Immediate IgG neutralization of all allergen
Direct cytotoxic killing of epithelial cells
Which statements correctly describe atopic individuals? Select all that apply.
They never mount secondary immune responses
They are described etymologically as out of place
They are defined as having altered reactivity
They have a predisposition to allergies
Which best characterizes the relationship between primary and secondary immune responses to allergens?
Primary exposure creates memory enabling stronger secondary
Secondary exposure is weaker due to lack of memory
Primary exposure eradicates allergen preventing any secondary
Secondary exposure induces tolerance reducing all symptoms
Which statement best links allergies to antiparasite immunity?
Allergies result from chronic bacterial biofilm immunity
Allergies develop from antibody responses against viruses
Allergies arise from immune pathways against helminths
Allergies are caused by autoimmune responses to self tissues
Where have epidemic rates of allergy become most prominent over recent decades?
Polar regions with minimal human population
Rural areas with high livestock exposure
Industrialized nations with low parasite exposure
Tropical regions with endemic helminth infections
According to the hygiene hypothesis, which combination most plausibly reduces early-life microbial exposures and shifts immunity toward allergy?
Frequent exposure to soil helminths
Regular personal hygiene behaviors
Widespread antibiotic treatments
Routine protective immunizations
Food and water sanitization practices
What is a proposed consequence when parasites are absent from the host during development?
Complement activation permanently replaces antibody functions
Th1 polarization increases and suppresses all infections
IgG responses dominate and prevent any allergic sensitization
IgE mechanisms lose natural targets and misfire on harmless antigens
Which tenet reflects a risk of overreliance on antibiotics within the hygiene hypothesis framework?
Increased exposure to diverse microbiota through infections
Improved tolerance to dietary antigens in early childhood
Enhanced maturation of memory B cells against helminths
Reduced immune discrimination between pathogens and commensals
Select the mechanisms most characteristic of IgE‑mediated hypersensitivity.
Complement MAC formation on parasite surfaces
Immediate degranulation releasing histamine
Cytotoxic CD8 T cell killing of epithelia
Eosinophil recruitment to affected tissues
Mast cell activation via FcεRI cross‑linking
Which statement best summarizes the developmental implication of the hygiene hypothesis?
Vaccinations directly cause allergic disease in every child
Childhood immune systems may be undertrained without real infections
Childhood immunity becomes stronger only with repeated antibiotics
Adult immunity cannot change after early-life microbial exposures
Which statement best describes why helminth infections tend to elicit a TH2-dominant adaptive immune response?
Helminths primarily infect bone marrow tissue
Helminths lack antigens recognizable by innate cells
Helminths are intracellular bacteria, favoring TH1
Helminths are larger than immune cells, favoring TH2
Which innate pattern-recognition pathways are highlighted for detecting parasite surface antigens, and which cells are directly involved?
Fc receptors on platelets
Scavenger receptors on erythrocytes
NOD-like receptors on dendritic cells
Toll-like receptors on macrophages
Which pairing correctly matches pathogen size with the predominant T-helper response?
Small intracellular pathogens – TH2 response
Large extracellular pathogens – TH2 response
Small intracellular pathogens – TH17 response
Large extracellular pathogens – TH1 response
Which functions are attributed to macrophages and dendritic cells during early responses to helminth antigens?
Dendritic cells endocytose and process antigens
Dendritic cells suppress T cell activation
Macrophages clear antigens and mediate inflammation
Macrophages activate B cells for antibody class switch
Which helminth group is primarily intestinal in humans as depicted in the diagram of worm types?
Thorny-headed worms prefer lungs
Roundworms avoid gastrointestinal sites
Flukes infect peripheral nerves
Tapeworms infect the intestines
Based on the helminth types image, which statement best matches flukes?
Mainly infect animals and never humans
Generally infect bile ducts, liver, or blood
Only cause infections in nasal passages
Exclusively infect skeletal muscle fibers
From the worm types shown, which category is noted as mainly infecting animals with rare human infection?
Tapeworms rarely infect any mammals
Roundworms mostly parasitize plants
Thorny-headed worms are mainly animal pathogens
Flukes never cross species boundaries
In the immune pathway diagram, which epithelial cell type is labeled as secreting mucins that support worm expulsion?
Paneth cells make collagen
Tuft cells release keratin
Enterocytes exude histamine
Goblet cells secrete mucins
Which cytokines are shown as being released by tuft cells to initiate type 2 responses?
IFN-γ
IL-12
TSLP
IL-33
IL-25
According to the pathway figure, dendritic cells activated by helminth antigens prime which T helper subset?
Th1 cells driving macrophage killing
Th17 cells promoting neutrophilia
Treg cells enforcing tolerance
Th2 cells mediating type 2 immunity
Which effector cells are depicted as downstream targets of IL-4, IL-5, IL-9, and IL-13 in helminth defense?
Mast cells
Eosinophils
Neutrophils
NK cells
Basophils
What is the illustrated role of dendritic cells at the intestinal barrier in helminth infection?
Phagocytose red blood cells for iron
Produce mucins to trap invasive larvae
Release histamine to paralyze helminths
Capture antigens and migrate to lymph nodes
Which event directly triggers degranulation of eosinophils, basophils, and mast cells during parasite defense?
TLR4 recognition of lipopolysaccharide endotoxin
IgE binding to FcεRI receptors on their surface
IgG3 binding to Fcγ receptors on neutrophils
Complement C3b deposition on parasite cuticle
A patient with helminth infection shows elevated eosinophils. Which cytotoxic eosinophil product is most associated with killing parasites and inducing mast cell histamine release?
TNF-α stored in mast cell granules
CXCL8 secreted by macrophages
Histamine released from basophils
Major basic protein in eosinophil granules
Which combination best describes eosinophil location and granule chemistry under steady state?
Splenic residents with immunoglobulin light chains
Marginal pool neutrophils with neutral proteases
Primarily circulating cells with acidic lysosomal enzymes
Mostly tissue residents with toxic alkaline proteins
Which eosinophil enzyme remodels connective tissue matrix rather than directly killing parasites?
Eosinophil collagenase acting on matrix proteins
Eosinophil peroxidase catalyzing halogenation
Eosinophil cationic protein as neurotoxin
Eosinophil-derived neurotoxin degrading RNA
Select all eosinophil products that can directly kill parasites or act as toxins.
Major basic protein causing parasite damage
Eosinophil-derived neurotoxin degrading RNA
Eosinophil cationic protein acting neurotoxic
CXCL8 chemokine recruiting leukocytes
Basophils are least abundant among granulocytes. Which feature is most characteristic of basophils in blood?
Dominant producers of IgG3 antibody
Agranular cytoplasm with few mediators
Large share of circulating leukocytes
Less than one percent of total white cells
Which statement best reflects a current understanding of basophil function?
Granules contain histamine and heparin mediating inflammation
They present antigen via MHC I to CD8 T cells
They suppress TH2 cells by IL-12 secretion
They phagocytose bacteria using oxidase-dependent killing
Basophils can promote humoral responses. Which property directly supports this role?
Secretion of perforin enabling cytolysis of targets
Expression of CD40 ligand supporting B cell activation
High-affinity uptake of IgG3 through FcγRIII
Production of IL-12 biasing TH1 differentiation
Which statement about FcεRI on basophils is most accurate?
Surface FcεRI holds specific IgE acting like memory
FcεRI prevents TH2 activation in later responses
FcεRI binds IgG subclasses with equal affinity
FcεRI is internalized permanently after binding
Mast cells are long-lived tissue residents. Which granule contents are typical and immediately mediating acute inflammation?
Defensins and myeloperoxidase from azurophils
Granzyme B and perforin from cytotoxic cells
Interferon-γ and IL-12 stored preformed
Histamine and degradative enzymes such as tryptase
Which pairing of mast cell subset and granule protease is correct?
Connective tissue mast cells store tryptase only
Connective tissue mast cells lack serine proteases
Mucosal mast cells contain tryptase in granules
Mucosal mast cells contain chymotrypsin alone
Which set of mast cell mediators most directly causes smooth muscle contraction, vascular permeability, and mucus secretion during helminth expulsion?
Leukotrienes C4 D4 E4 lipid mediators
Type I interferons alpha and beta
Chemokine CXCL8 recruiting neutrophils
Complement C5a and properdin proteins
Which cytokines from mast cells promote eosinophil production and activation from bone marrow during parasite responses?
IL-2 IL-7 and IL-15 expand T cells
TGF-β IL-10 and IL-27 dampen immunity
IL-3 IL-5 and GM-CSF support eosinophils
IL-12 IL-18 and IFN-γ drive TH1 cells
Which mediator stored or produced by mast cells promotes inflammation and activates endothelium to recruit leukocytes?
IL-4 exclusively stored as inactive pro-cytokine
Prostaglandins acting as antiviral cytokines
TNF-α produced and partly preformed in granules
Histamine only released after new synthesis
Which cytokine most directly drives eosinophilia in helminth infection as shown in the diagram?
TGF-β from Treg cells
IL-5 from Th2 cells
IL-4 from Th2 cells
IL-9 from Th2 cells
A dendritic cell presents helminth antigens to a naïve Th0 cell. Which differentiation pathway predominates to promote IgE production?
Th2 differentiation via IL-4
Th1 differentiation via IFN-γ
Treg differentiation via IL-10
Th17 differentiation via IL-6
Which pair of cytokines from Th2 cells increases mucus production and epithelial permeability, respectively?
IL-4 for mucus, IL-13 for permeability
IL-9 for mucus, IL-5 for permeability
IL-13 for mucus, IL-4 for permeability
IL-5 for mucus, IL-9 for permeability
Alternative macrophage activation (AAM) in helminth responses tends to inhibit which T helper subsets?
Th1 inflammatory cells
Th2 effector cells
Th17 inflammatory cells
Treg suppressor cells
During the immediate phase of an allergic reaction, which sequence best describes the key cellular events leading to symptoms?
AAM suppresses Th2 then fibrosis
B cells switch to IgG4 then quiescence
Neutrophils release IL-10 then tolerance
IgE binds mast cells then degranulation
Which mediator released from mast cells is depicted contributing to acute allergy symptoms?
IL-17 and GM-CSF
IFN-γ and TNF-β
Histamine and tryptase
IL-10 and TGF-β
In the late phase reaction, which cell–cytokine axis promotes resolution by dampening inflammation?
AAM macrophages via IL-10
Mast cells via histamine
Th1 cells via IFN-γ
Th17 cells via IL-17
Which is the correct relative affinity ranking for antibody isotypes as shown?
IgG3 = IgG2 < IgG4 < IgG1 < IgE
IgG1 < IgG3 < IgG4 = IgG2 < IgE
IgG4 < IgG2 = IgG1 < IgG3 < IgE
IgE < IgG3 < IgG1 = IgG2 < IgG4
Which mechanism best characterizes Type I hypersensitivity?
CD8 T cells kill hapten-modified cells
Immune complexes deposit in glomeruli
IgG binds drug on red cell surface
IgE on mast cells cross-links with allergen
A patient develops anaphylaxis minutes after a peanut exposure. Which immune event is most immediate?
Mast cell degranulation releasing mediators
Complement-mediated cell lysis of neutrophils
Granuloma formation via Th1 cytokines
Antibody class switching to IgA in mucosa
Which clinical trigger is most typical for Type II hypersensitivity?
Penicillin binding to erythrocyte membrane
Pollen inhalation during spring season
Nickel contact from a watch bracelet
Serum sickness after antitoxin therapy
In Type II hypersensitivity, what consequence follows antibody binding to a cell-associated hapten?
IL-4 driven class switching to IgE
Formation of circulating immune complexes
Immediate histamine release from basophils
Complement activation leading to phagocytosis
Which scenario illustrates Type III hypersensitivity most accurately?
Contact allergens activate cytotoxic T lymphocytes
Drug-modified cells targeted by IgG cytotoxicity
Allergen-specific IgE cross-links on mast cells
Small immune complexes deposit in capillaries
Which statements are correct about Type IV hypersensitivity? Select all that apply.
Involves cytotoxic T cells in some reactions
Driven by preformed IgE antibodies
Develops with a delayed time course
Mediated primarily by T lymphocytes
A healthcare worker develops a pruritic rash where a nickel ID clip contacts skin. Which mechanism explains this reaction?
Preformed IgE triggers immediate histamine release
Immune complexes deposit in dermal vessels
Nickel modifies self-proteins presented on MHC I
IgG binds nickel in serum causing hemolysis
Match each hypersensitivity type with a representative trigger.
Type II — penicillin-coated erythrocytes
Type I — plant pollen exposure
Type III — post-antitoxin serum sickness
Type IV — poison ivy urushiol contact
In the Type I panel, which immediate event is triggered when antigen cross-links IgE bound to FcεRI on a mast cell?
Degranulation with mediator release
Complement C3b deposition
Neutrophil extracellular trap formation
B cell class switching to IgM
Cytotoxic T cell perforin release
Which pairing best matches each hypersensitivity type with its principal effector or mechanism depicted?
Type I — IgE and mast cell activation
Type IV — Immediate complement-mediated lysis
Type III — Immune complexes recruiting neutrophils
Type IV — Sensitized T cells activating macrophages
Type II — IgG against drug-induced new epitopes
In the Type II sequence with penicillin, what creates the target for IgG binding on host cells?
Immune complex deposition in vessels
Superantigen activation of T cells
Viral antigen presentation on MHC I
Drug-modified surface forms new epitope
Preformed IgE on basophils cross-linking
The Type III panel shows infused mouse antibodies forming complexes. What downstream cellular responder is highlighted at the vessel wall?
Platelet aggregating via GP IIb/IIIa
NK cell mediating ADCC via CD16
Basophil cross-linking surface IgE
Eosinophil releasing major basic protein
Neutrophil engaging Fc and complement
Regarding timing and mediators, which statements are correct for the Type IV reaction shown?
Reaction is antibody-independent and T cell–mediated
Mast cell degranulation is the dominant event
Onset occurs some days after exposure
Effector cells are CD4 T cells and macrophages
Immune complexes drive neutrophil recruitment
Which clinical scenario best maps to the mechanism illustrated for Type I hypersensitivity?
Acute anaphylaxis after peanut ingestion
Hemolysis from penicillin-induced epitope
Serum sickness from heterologous antibodies
Contact dermatitis after nickel jewelry
Post-strep glomerulonephritis presentation
Which event defines sensitization during the primary response to an inhaled allergen such as pollen?
Eosinophils phagocytose airborne allergens
Mast cells degranulate and release histamine
TFH2 cells induce B cells to secrete IgE
Circulating IgG neutralizes inhaled pollen
During first exposure to pollen in the airway, which sequence best describes the cellular steps leading to mast cell arming?
APC activates TFH2, B cell secretes IgE
APC activates CTL, mast cells express Fcγ
B cell secretes IgG, mast cells bind IgG
TFH1 activates B cell, neutrophils bind IgE
Which receptor on mast cells binds allergen-specific IgE to arm the cell for subsequent reactions?
CD28 co‑stimulatory receptor
TLR4 endotoxin sensor
FcγRII low‑affinity IgG receptor
FcεRI high‑affinity IgE receptor
Which statements are true of type I hypersensitivity (allergic rhinitis) caused by inhaled pollen?
It is driven by TFH2 cell help for B cells
It is an immediate hypersensitivity reaction
It involves mast cell activation via IgE
It primarily relies on IgA neutralization
In acute allergic responses in the airway, mast cell mediators most directly cause which effects?
Increased mucus secretion by epithelium
Smooth muscle contraction in airways
Decreased blood vessel permeability
Rapid eosinophil apoptosis in tissue
Which component most increases during chronic allergic rhinitis compared with the acute phase?
NK cell cytotoxic granules
Complement membrane attack complex
Cytokine‑driven eosinophil products
Neutrophil extracellular traps
Which statement best differentiates primary from secondary immune responses to an allergen?
Primary activates CTLs; secondary activates macrophages
Primary arms mast cells with IgE; secondary triggers hypersensitivity
Primary causes degranulation; secondary causes IgE
Primary produces IgG memory; secondary produces naïve IgM
Which inhaled environmental allergen is most commonly associated with seasonal rhinitis in the United States?
Cat dander proteins
Airborne pollen allergens
Mold spore antigens
House dust mite allergens
Place these events in correct order for first pollen exposure leading to sensitization.
Mast cell degranulation, IgE secretion, TFH2 activation
Extraction of allergens, TFH2 activation, IgE secretion
IgE binds FcεRI, allergens extracted, TFH2 activation
TFH2 activation, IgE secretion, allergen extraction
Which cell type provides help to B cells that is specifically linked to class switching to IgE during allergen sensitization?
TFH2 helper T cells
TH1 helper T cells
Regulatory T cells
Cytotoxic T lymphocytes
