Hypersensitivity Flashcards
What is hypersensitivity?
Exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage
IgE is really responsible for a lot of allergic reactions. Check out slide 5 of the lecture for a table to know
okay
In order for type I hypersensitivity to occur, what must happen first?
A prior exposure to the allergen must have happened for hypersensitivity to occur.
What is the initial exposure to an antigen and subsequent production of IgE called?
Sensitization
IgE is made in response to some cytokines. What does IgE bind to that causes the hypersensitive reaction?
IgE binds to mast cells, which degranulate and cause a bisphasic response
What are the immediate and late effects of mast cell degranulation (release of mediators)?
Immediate effects: dilation of blood vessels, increased vascular permeability, and smooth muscle contraction
Late effects: inflammation
What do prostaglandins do?
Vasoconstriction in the lungs
What do leukotrienes do?
bronchoconstriction and increased vascular permeability
What is contained in the granules released by eosinophils?
ROS
major basic protein
prostaglandins and leukotrienes
What are the most common signs/symptoms of asthma?
coughing, wheezing, and shortness of breath
What are some common asthma triggers?
airborne allergens like pollen, animal dander, mold, cockroaches, and DUST MITES respiratory infections physical activity cold air air pollutants
What do ITAMs do?
They activate map kinase
What enzyme do dust mites have that cleaves the tight junctions of respiratory epithelium? Then what happens?
It’s called Der p1 and it cleaves the occludin protein
Then the dust mite gets taken up by an APC and the specific IgE binds a mast cell and degranulation takes place
During asthma, mucous is produced and muscles often become thickened, but constricting the airways
indeed
What are two treatment strategies for asthma? What do they do?
Inhaled corticosteroids- relieve airway inflammation and swelling
Leukotriene modifiers-help block the chain reaction that increases inflammation in the airways
T/F the dose and routes of entry of allergens determine the type of IgE mediated allergic reaction that results
true
What is an example of a wheel and flare reaction?
A hive
When a mast cell degranulates, what molecule is responsible for vascular leakage?
histamine
When a mast cell degranulates, what molecule is responsible for intestinal hypermotility?
lipid mediators
When a mast cell degranulates, what molecule is responsible for tissue damage?
enzymes
When a mast cell degranulates, what molecule is responsible for inflammation?
cytokines
T/F all clinical and pathological features of immediate hypersensitivity reactions are driven by mediators produced by B cells?
False- mediators produced by mast cells
What is the most severe form of immediate hypersensitivity?
Anaphylaxis
An anaphylactic reaction is driven by the systemic release of what?
vasoactive amines (histamines) and lipid mediators from mast cells
Why is anaphylaxis so deadly?
It causes a life-threatening drop in BP and is accompanied by severe bronchoconstriction
How is anaphylaxis treated?
epinephrine and antihistamine injection
Cytokine release recruits what to where?
eosinophils and neutrophils to the site of inflammation
What is type II hypersensitivity?
Where antibodies produced by the immune system bind to antigens on our own cell surface or bind self antigens and can activate the complement cascade and kill our cells
What happens in hemolytic disease of the new born?
Maternal antibodies target fetal RBCs for destruction
What happens in hemolytic anemia?
Auto-antibodies are produced against self antigens on the surface of RBCs. This triggers the rapid destruction of RBCs, leading to anemia
What happens in hemolytic disease of the new born?
Maternal antibodies target fetal RBCs for destruction (opsinization of RBC’s)
What happens in hemolytic anemia?
Auto-antibodies are produced against self antigens on the surface of RBCs. This triggers the rapid destruction of RBCs, leading to anemia (opsinization of RBC’s)
What happens in graves disease?
TSH receptor antibodies stimulate TSH receptor to over produce thyroid hormone
What happens in myasthenia gravis?
Ach receptor antibodies bind to and block the Ach receptor
What is type III hypersensitivity?
Ag-Ab complexes clump and deposit in blood vessels or tissues attracting an acute inflammatory reaction
In type III hypersensitivity, what happens to larger and smaller complexes/aggregates?
Larger aggregates are cleared from the circulation by phagocytes
Smaller complexes formed in Ag excess are deposited in blood vessels or tissue
How quickly does type III hypersensitivity occur?
3-10 hours
What are the three ways that immune complexes trigger inflammation?
- Mast cell activation
- Macrophages release TNF-alpha and IL-1 that induce the inflammatory cascade
- C3a, C4a, and C5a stimulate mast cells to release more histamine, serotonin and chemotactic factors-also attracts monocytes, neutrophils, and other leukocytes
