Comprehensive GI Tract, Digestion, Absorption,
Pancreas, Liver, Bile, Saliva, Stomach Acid,
Hormones, Enteric Nervous System, Immune
System, Hypersensitivity, Autoimmunity, T-Cells, B-
Cells, Mast Cells, Cytokines, Antibodies, Vaccines,
Cancer Immunology – High-Yield Exam Notes
Questions Verified and Provided with Complete A+
Graded Rationales Latest Updated 2026
What antibody is associated with type 1 hypersensitivity?
IgE
What are the two phases of type 1 hypersensitivity?
1. Sensitization
2. Effector (re-exposure)
What is the main cell involved in Type 1 hypersensitivity?
Mast cells
Sensitization phase of Type 1 hypersensitivity
1. Allergen is captured by the DC and processed to activated TH2 cell
2. Th2 cell releases IL-4
3. IL-4 = IgE production
4. IgE will then go and bind to the FceR on the mast cell
- ↑ FceR affinity for IgE
- will hang out here and bind in absence of antigen
In type 1 hypersensitivity, the allergen activates what type of T-cell?
Th2
- will go on to release IL-4 and release IgE to bind to FceR on mast cells
Where is the FceR receptor found?
on the MAST CELL
1|Page
,Th2 cells release _________
IL-4 cytokine and activate B cells to produce IgE; activate eosinophils
Effector Phase of Type 1 hypersensitivity
Re-Exposure of the allergen
1. allergen binds to the IgE bound to the FceR on the mast cell
2. CROSSLINKING occurs across IgE to initiate the mast cells to degranulate
3. Mast cells degranulate and release primary mediators from granules: histamine, heparin,
tryptase.
4. Secondary mediators are synthesized and released: prostaglandins, leukotrienes
What are the primary mediators released by mast cells?
histamine
tryptase
heparin
histamine affect as a primary mediator
↑ vasodilation
↑ vasopermeability
↑ bronchoconstriction
↑ itch/cramps/diarrhea
tryptase affect as a primary mediator
↑ MMPs (make path for cells to get into ECM)
↑ itch
Heparin affect as a primary mediator
↑ bradykinin = ↑ vasodilation
Prostaglandin affect as a secondary mediator
↑ vascular permeability
↑ bronchoconstriction
↑ PMN recruitment
Leukotriene affect as a secondary mediator
↑ mucus production
2|Page
, POTENT
↑ antibody production via IL-4 and IL-13
↑ IL-5 (eosinophils)
Which secondary mediator is responsible for mucus increased during a type 1 hypersensitive
reaction?
leukotrienes
Inhibit with Montelukast (Singulair)
What meds are good for blocking leukotriene affect?
Montelukast (Singulair)
- leukotriene receptor antagonist
allergic rhinitis, asthma, food allergies, urticaria (hives), systemic anaphylaxis = ___________
hypersensitivity
type 1 hypersensitivity
systemic anaphylaxis
high levels of IgE bound to FceR on mast cells and basophils (blood) = systemic degranulation
- affects tissues, lungs, cardio
- EMERGANCY
Treatment:
- epinephrine
What is given to resolve systemic anaphylaxis?
EPINEPHRINE
- potent vasoconstrictor
(↑ BP, ↑ HR, reduce shock, ↑ cAMP)
**anti-histamine acts TOO SLOW**
How do allergy shots work?
changing response from IgE to IgG4
- this will win out and shut down degranulation
3|Page
Pancreas, Liver, Bile, Saliva, Stomach Acid,
Hormones, Enteric Nervous System, Immune
System, Hypersensitivity, Autoimmunity, T-Cells, B-
Cells, Mast Cells, Cytokines, Antibodies, Vaccines,
Cancer Immunology – High-Yield Exam Notes
Questions Verified and Provided with Complete A+
Graded Rationales Latest Updated 2026
What antibody is associated with type 1 hypersensitivity?
IgE
What are the two phases of type 1 hypersensitivity?
1. Sensitization
2. Effector (re-exposure)
What is the main cell involved in Type 1 hypersensitivity?
Mast cells
Sensitization phase of Type 1 hypersensitivity
1. Allergen is captured by the DC and processed to activated TH2 cell
2. Th2 cell releases IL-4
3. IL-4 = IgE production
4. IgE will then go and bind to the FceR on the mast cell
- ↑ FceR affinity for IgE
- will hang out here and bind in absence of antigen
In type 1 hypersensitivity, the allergen activates what type of T-cell?
Th2
- will go on to release IL-4 and release IgE to bind to FceR on mast cells
Where is the FceR receptor found?
on the MAST CELL
1|Page
,Th2 cells release _________
IL-4 cytokine and activate B cells to produce IgE; activate eosinophils
Effector Phase of Type 1 hypersensitivity
Re-Exposure of the allergen
1. allergen binds to the IgE bound to the FceR on the mast cell
2. CROSSLINKING occurs across IgE to initiate the mast cells to degranulate
3. Mast cells degranulate and release primary mediators from granules: histamine, heparin,
tryptase.
4. Secondary mediators are synthesized and released: prostaglandins, leukotrienes
What are the primary mediators released by mast cells?
histamine
tryptase
heparin
histamine affect as a primary mediator
↑ vasodilation
↑ vasopermeability
↑ bronchoconstriction
↑ itch/cramps/diarrhea
tryptase affect as a primary mediator
↑ MMPs (make path for cells to get into ECM)
↑ itch
Heparin affect as a primary mediator
↑ bradykinin = ↑ vasodilation
Prostaglandin affect as a secondary mediator
↑ vascular permeability
↑ bronchoconstriction
↑ PMN recruitment
Leukotriene affect as a secondary mediator
↑ mucus production
2|Page
, POTENT
↑ antibody production via IL-4 and IL-13
↑ IL-5 (eosinophils)
Which secondary mediator is responsible for mucus increased during a type 1 hypersensitive
reaction?
leukotrienes
Inhibit with Montelukast (Singulair)
What meds are good for blocking leukotriene affect?
Montelukast (Singulair)
- leukotriene receptor antagonist
allergic rhinitis, asthma, food allergies, urticaria (hives), systemic anaphylaxis = ___________
hypersensitivity
type 1 hypersensitivity
systemic anaphylaxis
high levels of IgE bound to FceR on mast cells and basophils (blood) = systemic degranulation
- affects tissues, lungs, cardio
- EMERGANCY
Treatment:
- epinephrine
What is given to resolve systemic anaphylaxis?
EPINEPHRINE
- potent vasoconstrictor
(↑ BP, ↑ HR, reduce shock, ↑ cAMP)
**anti-histamine acts TOO SLOW**
How do allergy shots work?
changing response from IgE to IgG4
- this will win out and shut down degranulation
3|Page
