Hypersensitivity Rxns Flashcards
what is a hypersensitivity run and what do they require
Over rxn of the immune system to self or non self antigens
-require a sensitized host (prior exposure)
What are type 1 hypersensitivities mediated by
IgE mediated
-soluble antigens cross link IgE antibodies bound to mast cels/basophils
examples of type 1 hypersensitivites (4)
atopy
allergies
acute allergic asthma
anaphylaxis
How are IgE antibodies developed : what cells stim them and ILs needed
B cells stimed by Th2 cells
need IL4,5,13
Steps to get mast cells sensitized
- APC present to Th2
2.Th2 acctivate b cells - B cells proliferate into plasma cells and secrete IgE
4 IgE bind to mast cells sensitizing them
What does reexposure to antigens bind to
preexposure of certain antigens bind IgE and crosslink FceRI receptors
What is released in the immediate type 1 hypersensitivity and what occurs (2)
immediately after exposure histamine and leukotriene released which causes: vasodilation of arterioles and increased permeability, airway smooth mm contraction, leukocyte extravasation to affected site
When does late phase type 1 hypersensitivity occur and what is released
2-6 hrs post
-cytokines (IL4,5,13) amplifies type 1 rxn (activate eosinophils, neutrophils, monocytes etc)
Natural hx of type 1 hypersensitivity
12hrs- 3days
acute rxn
What percentage of people have atopy and why
10-20%
-higer total lvl of IgE in circulation, more eosinophils
What is the clinical manifestation to atopy
allergy
What leads to atopy
- genetics (components of immune system)
- Environment (infection)
- Lifestyle (stress, obesity)
What is allergy mediated by
IgE antibodies
Effect of type 1 hypersensitivity on nasal passages and eyes
eyes: redness, itchy, watery eyes, conjunctiva
nasal: allergic rhinitis, sneezing, runny nose, coughing etc, respiratory distress etc
What is asthma
disease of the bronchi and bronchioles causing attacks/paroxysms of reversible airflow obstruction (airway inflammation, bronchospasm, mucus hyper production)
What are the primary clinical manifestations on the skin of type 1 hypersensitivities
- dermatitis (eczema)- red area of superficial skin that is often itchy
- Urticaria (hives)- raised areas surrounded by a red base, itchy, typically lasts <24hrs
Food allergy vs food intolerance
allergy- IgE mediated process
intolerance- IgG mediated process
What is anaphylazis and how is it mediated
IgE mediated- widespread basophil degranulation+ systemic inflammation
-itchy hives,dyspenia, light-headedness, low bp
common characteristics of allegens (5)
- low molecular weight
- highly soluble
- multivalent antigens
- enzymatically active
- stable chem structue
What is the major allergen of house dust mite and what does it do
Der p1
Break up tight junctions getting increased access to APCs in mucosal tissues
Gold standard of allergy testing
blood testing: cells timed with antigen under investigation and IgE antibodies measured
What are drugs to treat allergies
Antihistamines Leukotriene inhibitors Inhaled bronchodialators Epinephrine- relaxes sm mm Allergy shots- (expand tolergenic responses)
What are type II hypersensitivities mediated by
IgG or IgM antibodies directed against cell associated antigens or ECM antigens
What do type II hypersensitivities result in
Cytotoxic responeses
- activation of classic complement path
- antibody dependent cell mediated cytotoxicity
- Phagocytosis
What are isoantibodies
IgM/IgG antibodies against blood antigens you don’t have
What do isoantibodies do when blood is mismatched (3)
- Agglutination
- Clumps activate classical complement pathway
- Hemolysis by MAC/inflammation/opsinization
When does hemolytic disease of the fetus and newborn occur
if mother is rh- and child is rh+, mother may generate anti rh IgG antibodies and if next child is rh+ it will initiate hemolytic rxn
what occurs in myasthenia gravis
type II hypersensitivity
IgG autoantibodies target nicotinic act receptors on neuromuscular junction blocking action pot/ activate classical complement pathway
What occurs in Graves disease
Type II hypersensitivity
-autoimmune disorder where IgG antibodies bind to thyroid stem hormone receptor causing over prod of T3/T4 (hyperthyroidism)
Symptoms of Graves disease
Unexplained weight loss, elevated HR, high BP, anxiety/irratability etc
What are type III hypersensitivities and what do they activate
formation of small immune complexes between IgG antibodies and soluble antigens (deposits in walls of blood v)
-activate classical complement pathway, inflammation
What is arthur’s reaction and serum sickness due to and what do they do
type III hypersensitivity
-small immune complexes in tissues causing inflammation/tissue damage
Arthus- localized
serum- systemic
What is systemic lupus erythematosus and what causes it
Type III hypersensitivity (IgG autoantibodies and soluble nuclear antigens)-deposit in tissues and activate complement/inflammation
-fatiue, fever, jt pain/swelling, rashes, any organ targeted
What is required for a type 4 hypersensitivity and timeframe
- delayed hypersensitivity (>24hrs)
- Requires prior exposure to antigen and sensitization to generate antigen specific t cells
What type of antigen specific t cell is required for TB type 4 hypersensitivity
Th1 cells
What type of antigen specific t cell is required for chronic asthma and what does it cause
Th2 cells
-airway remodelling, hyperresponsitivness (to irritation) and obstruction
What type of antigen specific t cells are required for poison ivy (type 4) and what do each do
th1 cells= activate macrophages
clts- induce apoptosis
