14 - Allergy and Hypersensitivity Flashcards
What are hypersensitivities?
inappropriate immune response to antigens that pose little to no threat
Which antibodies are responsible for Type I hypersensitivities?
IgE antibodies
What are allergies initiated by?
interaction between an IgE and a multivalent antigen
What are the 6 common allergic reactions?
hay fever | asthma | eczema | bee stings | hives | food allergies
What are atopic individuals?
people who are susceptible to allergens
What is IgE only supposed to respond to?
pathogens specifically parasitic infections
What are 2 properties of allergens?
enzymatic protease = break through barriers | PAMPS = trigger activation and immune system
What are allergens?
non-parasitic antigens
In Type I hypersensitivity reactions, how do IgE antibodies act?
IgE = bound to mast cells | cross-linking Fce receptors on surfaces of innate immune cells (mast cells) = degranulation
What are in the granules of granulocytes?
histamine | heparin | proteases | leukotrines | prostaglandins | chemokines
If there is no allergen present during degranulation, what will happen to the contents of the granules?
will impact the tissue it is near = cause inflammation
What is the Fc receptor involved in Type I hypersensitivity?
FceR
On which cells are FceR only found on?
mast cells | eosinophils | basophils
What does histamine cause?
contraction of intestinal and bronchial smooth muscles | mucus secretion | increase vasopermeability and vasodilation | mast cell chemotaxis
What do prostaglandins and leukotrienes cause?
vascular permeability | mucus secretion | major cause of asthma symptoms
In Type I hypersensitivity, what does IL-5 do?
recruits and activates eosinophils
In Type I hypersensitivity, what does TNFa do?
contribute to shock in systemic anaphylaxis
What is CXCL-8?
chemotactic factor
In Type I hypersensitivity, what does IL-13 do?
helps with mucus secretion, goblet cells, hyperplasia
In Type I hypersensitivity, what does GM-CSF do?
helps with production of granulocytes
What is the early response during a Type I hypersensitivity reaction?
mast cells induce vasodilation | bronchoconstriction and goblet cells produce mucus = hard to breathe
What is the late response during a Type I hypersensitivity?
more cells and inflammation to surrounding tissue | chemokine and cytokine production | eosinophil recruit neutrophils and induce degranulation
What are the 3 categories of Type I hypersensitivity reactions?
systemic anaphylaxis | localized hypersensitivity reactions | food allergies
What are 2 symptoms of systemic anaphylaxis? What is the treatment?
drop in BP = leads to shock | smooth muscles contract = bronchoconstriction | Tx = epinephrine
What is the basis or cause for Type I hypersensitivity?
environmental factors | hygiene hypothesis | genetic factors
What is the main idea of the hygiene hypothesis?
using Th2 cells at a younger age would help the body balance the Th1 response with Th2
How can genetics cause Type I hypersensitivity?
increased IgE production and more of a Th2 response
Which Th subsets counteract Th2 responses?
Treg and Th1
What are the 2 diagnostic methods used for Type I hypersensitivity reactions?
skin test | allergen-specific IgE levels in serum
What are 2 treatments for Type I hypersensitivity?
antagonists for the granule contents (anti-histamines, etc) | desensitization immunotherapy
What is desensitization immunotherapy?
induce Th1 and Treg responses
What is Type II sensitivity involved with?
complement activation (mostly) | ADCC = antibody-dependent cell cytotoxicity and NK cell-mediated
What causes Type II sensitivity reactions?
blood incompatibilities such as transfusion reactions, autoimmune hemolytic anemia, HDN
What are blood group antigens made out of?
carbohydrates
How are antibodies involved with blood typing and how can this result in a Type II hypersensitivity reaction?
adults have antibodies against the blood group antigen they DON’T have
Which is the universal blood group donor?
O
Which is the universal blood group acceptor?
AB
What is the hemolytic disease of a newborn (HDN)?
when mom is Rh- but baby is Rh+ = mom’s Abs will attack baby’s Rh+ RBCs | 2nd pregnancy = kills fetus
What is the treatment for HDN?
UV lights = breaks down bilirubin
What is a preventive measure for HDN?
rhogam shot = IgG abs against Rh-factor
What is responsible for Type III hypersensitivity?
immune complexes = Ag/Ab complexes | complexes usually get cleared after a while if no autoimmune disease or drug inducing it to stay
What does Type III hypersensitivity cause?
complement activation = inflammation and recruitment of neutrophils
What are 3 key symptoms of Type III hypersensitivity?
joint pain due to complex deposits | proteinuria (protein in urine) | hematuria (blood in urine) due to complexes stuck on kidneys
What can induce Type III hypersensitivity reactions?
autoimmune diseases | drug reactions | infectious diseases
What is responsible for Type IV hypersensitivity reactions?
cell-mediated, initiated by T-cells, Th1 cells involved
What is Type IV sensitivity also called?
delayed type hypersensitivity = needs time for the reaction to develop about 1-2 weeks
What is Type IV hypersensitivity characterized by?
recruitment of macrophages at the inflammation site
What is the most common example of Type IV hypersensitivity?
poison ivy contact dermatitis
Why are macrophages important for Type IV hypersensitivity reactions?
macrophages = responsible for the inflammation
What is the early phase of Type IV hypersensitivity reactions?
sensitization phase = initiation of reaction involves sensitization by antigen = trigger T-cell (Th) response
What is the late phase of Type IV hypersensitivity reactions?
second exposure of antigen = induction of Th1 inflammatory cytokines = activate macrophages = granuloma formation
