Allergy, Hypersensitivity, and Chronic Inflammation Flashcards
Hypersensitivity definition
Failure of tolerance- inappropriate, vigorous innate and adaptive responses to antigen
Type 1 hypersensitivity: mediator and symptoms
IgE
Anaphylaxis, hay fever, asthma, hives, food allergies, eczema
Does an IgE response happen during a first or secondary exposure?
Secondary- first exposure doesn’t trigger reaction
Type of receptor that IgE acts upon
Fc eta receptors
Present on surfaces of immune cells
Two types of Fc eta receptors
High affinity: Fc eta R1
Low affinity: Fc eta R2
Differences between Fc eta R1 and Fc eta R2
Fc eta R1: responsible for most allergy symptoms, expressed by mast cells and basophils
Fc eta R2: regulates production of IgE by B cells
Result of binding to Fc eta R1
Degranulation and release
Formation and secretion of mediators such as histamine and cytokines
Type 1 hypersensitivity: early response
Occurs within minutes of allergen exposure
Mediated by mast cell granule release of histamine, leukotrienes, and prostaglandins
Type 1 hypersensitivity: late response
Hours after allergen exposure
Influx of neutrophils, eosinophils, and TH2 cells
Diagnosis of Type 1 reaction
Skin test: look for localized reaction to allergen
Treatment of type 1 hypersensitivity
Antihistamines
Leukotriene antagonist (targeting secondary mediator)
Steroids (asthma)
Immunotherapy: anti-IgE antibody
Hyposensitization
Treatment for type 1 hypersensitivity
Switching IgE response to IgG response by injecting small amounts of allergen
Hygiene hypothesis
Exposure to some pathogens early in life provides a better T-cell balance (less TH2, which promotes IgE production)
High incidence of allergy and asthma in developed countries, but lower in farm environment
Type 2 hypersensitivity: mediator
Antibodies (other than IgE) bind to antigens on person’s own cell surfaces
Antibody bound to cell surface antigen can induce cell death in what 3 ways?
- Complement activation/ MAC
- Cytotoxic cells bind to antibodies on target cell and promote killing
- Opsonization: mediate phagocytosis by phagocytes
Conditions in which type 2 hypersensitivities occur
Transfusion reactions: receiving infusion of non-matching blood type
Hemolytic disease of newborn: Rh negative mother mounts immune response against Rh positive fetus
Drug-induced hemolytic anemia: antibiotics such as penicillin, cephalosporin, and streptomycin attach to proteins on red blood cells, stimulating complement-mediated destruction
Which types of hypersensitivities can penicillin induce?
All 4
Type 3 hypersensitivity: mediator
Immune complexes: antigen/antibody complexes deposited in tissues induce complement activation and inflammation due to influx of neutrophils
Symptoms of type 3 hypersensitivity
Fever, rashes, joint pain, lymph node enlargement
Serum sickness
Type 3 hypersensitivity
Treatment with antibody serum can lead to systemic immune complexes against the treatment
Arthus reaction
Type 3 hypersensitivity
Swelling and localized bleeding
Caused by injection of antigen in person with high levels of circulating antibody specific to it
Type 4 hypersensitivity: mediator
T cells
Type 4 hypersensitivity: mechanism
1st exposure produces memory T cells
2nd exposure produces effector cells
Effector cells release cytokines which activate macrophages and other inflammatory mediators
Type 4 hypersensitivity: symptoms
Usually contact dermatitis
Common inducers of type 4 hypersensitivity
Poison ivy
Solvents
Cosmetics (hair dyes)
Metals (Ni)
Delayed type (type 4) hypersensitivity: TB test
Secondary exposure to sensitizing antigen
Prolonged inability to clear antigen: TB-positive individuals
