Hypersensitivity Flashcards
What is Type I hypersensitivity?
Immediate (anaphylactic) hypersensitivity
What is Type I hypersensitivity mediated by?
IgE
What is a common name for type I sensitivity
allergies and atropic disorders
What are some examples of common antigens that are allergens?
Pollen, insect venom, foods, drugs, plant oils, metals
What cytokine is important in the IgE response of Type I hypersensitivity?
IL-4
Which T helper environment favors the development of allergies?
Th2
What do mast cells contain?
1- enzymes
2- toxic mediators that increase vascular permeability and cause SM contraction
3- cytokines (TNF alpha) that promote inflammation and stimulate other cytokine production
4- chemokines (CCL3) to promote the influx of monocytes and macrophages and neutrophils
5- lipid activators (leukotrienes) cause smooth muscle contraction and increase vascular permeability
Describe an Atopic individual:
Individuals genetically susceptible and generally have higher levels of IgE and eosinophils
What are chemokines?
to promote the influx of monocytes and macrophages and neutrophils
Describe the phases of a Type I reaction:
2 Phases:
- immediate phase (action of pre-formed mediators)
- late phase (cellular infiltration)
Does the first exposure to an allergen create a hypersensitivity reaction?
no
Describe the initial sensitization to allergens in Type I reactions
1- exposure to antigen
2- antigen activation of Th2 cells and stimulation of IgE class switching in B cells
3- production of IgE
4- IgE binds to mast cells
These mast cells are now sensitized because they have IgE bound to them
What happens when an antigen binds IgE on a mast cell?
Degranulation of mast cell
What causes the late phase reaction in Type I?
TNK alpha plays a big role
What is the Hygiene hypothesis?
Suggests that the incidence of alergies has doubled over the past 10-15 years possibly due to better and increased hygeine which has resulted in less exposure to pathogens, whiich skews immune responses to Th2 instead of Th1
How is Type I hypersensitivity treated?
1- avoidance of the allergen
2- use of drugs that reduce the symptoms (anti-histamines)
3- desensitization to allergen
4- allergic peptide vaccination
What is Type II hypersensitivity?
Antibody-mediated (Cytotoxic) Hypersensitivity
When do Type II reactions occur?
after antibody is bound to cellular proteins
What do bound antibodies initiate in Type II reactions?
inflammatory responses in tissue
For type II reactions, why are antibodies made?
May be produced because cell proteins have been altered
What other granulocytes are involved in Type I? When are they activated?
Eos and Baso. Degranulate after they are activated by the immune response.
What is an example of a Type II reaction?
hemolytic anemia, where the production of anti-RBC antibodies can result in destruction of RBC. results in lysis or phagocytosis of RBCs because compliment is activated
happens in mis-matched blood transfusions
How are Type II, Type III and Type IV treated?
1- avoidance of the antigen
2- reduction of the impact of the immune response to the antigen with non-steroidal and steroidal anti-inflammatory
3- reduction of the immune response in general or specifically
4- induction of regulation response (T regs)
5- blocking of the effector mechanisms or allergic response-cytokines, co-stimulatory molecules
What granulocyte is important for making mucous?
Eosinophils
When can chronic asthma occur? What is it mediated by?
in the presence of allergin and without the presence of allergin
it is mediated by cytokines and eosinophil products
Describe allergic asthma:
1-allergin capture
2- crosslinking of IgE on the mast cells
3- degranulation and releasing mediators that cause changes
4- Th2 cells that produce IL-13 (mucous production)
What is the immune reactant for Type II? And what does it do?
IgG. They fix compliment.
Which reaction results in autoimmune diseases?
Type II (antibodies target cell surface receptors)
What is Type III hypersensitivity?
Immune-complex mediated hypersensitivity
What causes Type III?
The deposition of persistent immune complexes of IgG and soluble antigens that are compliment fixing
What are the qualities of IC that determine their pathogenicity?
1- size 2- isotype 3- valency 4- charge 5- ability to fix compliment
Where are the common sites of IC deposition? And what does these sites determine
1- intravenous
2- subcutaneous
3- inhaled
These sites determine the clinical manifestation
Genetic component to asthma?
MHC genes, TCR genes, Th1 and Th2 regulation, IL-4 (anything that accefts expresion of IL-4 can lead to a predisposition)
Give three examples of Type III hypersensitivity
1- Serum sickness
2- post-streptococcal glomerulonephritis
3- arthus reaction
Explain how serum sickness is Type III hypersensitivity?
Response occurse after the development of antibodies to large amounts of foreign protein
What is Type IV Hypersensitivity?
Delayed (Cell mediated) hypersensitivity
What is Type IV mediated by?
Antigen-specific Th1 cells
When does Type IV occur?
1-3 days after exposure
What are the commonalities between Types II- IV?
May occur in response to foreign antigen
Also when an individual’s immune system reacts against autologous (self) or modulated self antigens autoimmunity.
Impacted by genetic susceptibility and environmental factors
How much more antigen is needed for Type IV vs Type II?
Type IV needs 100-1000X more
What are some examples of Type IV?
1- Delayed-type hypersensitivity
2- Contact hypersensitivity
3- Celiac disease
What is the effector cell of Type III?
IgG
