Hypersensitivities Flashcards
Type I: Immediate-type hypersensitivity reactions
initiated by mast cell degranulation mediated by cross-linking of IgE to IgE fc receptors on mast cells
reactions occur within minutes
Type II: altered self hypersensitivity reaction
initiated by allergen-specific IgG antibodies and inflammation is mediated by the complement cascade, phagocytes, and NK cells
takes 4-12 hours usually
Type III: Immune complex hypersensitivity reaction
result from immune complex deposition into host tissues and the inflammatory responses that ensue when phagocytes try to clear the complex
end result is inflammation that is driven by complement activation and phagocyte-derived cytokines and chemokines
type II can sometimes develop into Type III
(IgG is the immune reactant in this case as well)
Type IV: Delayed type hypersensitivity reaction
hypersensitivity response mediated by T cells (CD4 CD8 or both)
takes 24-72 hours
T/F There must be a first exposure to the allergen in which the primary immune response is generated, but no symptoms of hypersensitivity are experienced. After that, any subsequent exposure to that allergen elicits the hypersensitivity response and any symptoms that go along with that response.
true
Allergens that elicit IgE response and thus immediate-type hypersensitivity reaction
- must be proteins (must be proper T dependent cell antigens)
- often proteases
- low dose (driver differentiation from Th0 to Th2 needed for class switching to IgE)
- low molecular weight (can better diffuse out of dust particle)
- high solubility (will elute more efficiently from dust particle)
- highly stable (must survive as desiccated particle)
- contain peptide that binds to MHC class II
Mast cell granules
- tryptase, chymase, cathepsin G, carboxypeptidase-remodel connective tissue matrix
- histamine***, heparin-increase vascular permeability,cause smooth muscle contraction, toxic to parasites
- TNF-alpha (some stored preformed in granules)-promotes inflammation, stimulate cytokine production, activates endothelium
- IL-4, IL-13-stimulate and amplify Th2 response
- Leukotrienes C4, D4, E4-smooth muscle contraction, increase vascular permeability, mucus production
wheel and flare reactions
hives
primary role of mast cells
expulsion of parasites from the body
mast cell degranulation in the GI tract
increased fluid secretion and peristalsis leading to vomiting and diarrhea to clear the upper and lower GI tract
mast cell degranulation in the airway
increased mucus secretion and decreased diameter of the airways leading to coughing and sneezing to clear the airway
mast cell degranulation in the blood
vascular endothelium activated causing fluid and proteins to move from the vasculature into the inflamed tissue pushing fluid containing antigens and APCs from the lymph to the secondary lymphoid tissues where T and B cells can become activated
systemic degranulation of mast cells (anaphylactic shock)
- life threatening
- occurs if allergen gets into blood and is disseminated throughout the body
- causes rapid loss of blood volume leading to systemic edema and hypotension
- in the airway it causes contraction of smooth muscles and a compromised airway
- contraction in the GI tract leads to vomiting and diarrhea and further loss of fluids
- culminated in ANAPHYLACTIC SHOCK
treatment for anaphylactic shock
epinephrine/adrenaline
reverses the effects of mast cell degranulation on vascular epithelium
fecal matter of dust mites is an abundant source of______
proteolytic enzymes leading to mast cell response
most noteable type II hypersensitivity reactions
abnormal response to penicillin-modified erythrocytes following treatment with penicillin
type II hypersensitivity: penicillin-induced
- some penicillin binds to RBC’s and modified surface determinants
- complement cascade already initiated bc of ongoing infection so some C3B will be deposited on RBCs and macrophages will phagocytose
- macrophages can then present the altered determinants of RBCs to T cells
- T cells then activate B cells resulting in an antibody response against the altered RBC determinants
- antibodies bind to RBCs opsonizing them, and if the antibody isotype is one that fixes complement, RBCs will become coated with abundant C3b and will either be destroyed by MAC or taken up by phagocytes.
T/F destruction of RBCs following penicillin treatment will occur until the altered determinants have been recycled off the surface of the RBCs
true
Arthus Reaction
subcutaneous
- occurs when an allergen is introduced into tissues underlying the epithelium
- antibodies specific for the allergen activate the classical complement cascade
- resultant anaphylatoxins mediate inflammation directly and also binds to the C5a receptors on the mast cells underlying the epithelium
- results in mast cell degranulation (macrophages and neutrophils can also contribute to inflammatory response)
systemic immune response disease
intravenous
- allergen gains access to the vasculature and a large (too large to be cleared) number of immune complexes ensue
- these become deposited along the vasculature and especially in the glomeruli of the kidneys
- inflammatory mediators result from the production of anaphylatoxins and phagocyte mediators
- results in vacillates, kidney dysfunction, and neurologic symptoms resulting from vasculitis in the brain
- PRESENTATION SIMILAR TO SEPTIC SHOCK
farmer’s lung
inhaled
Immune complex hypersensitivities that result from inhalation of allergen
- inhaling mold spores and other allergens from hay
- occurs because pt works with the allergen daily
Pigeon breeder’s disease, poultry workers lung, bird breeders disease
all names for a condition that results from inhaling allergens that are found in the droppings of birds
delayed type hypersensitivity reactions
- most often mediated by Th1 cells and stimulates their effector responses
- chemokine production
- macrophage activation via IFN-gamma
- TNF-alpha and LT production to mediate local tissue destruction and increased expression of adhesion molecules
- IL-3 and GM-CSF production to increase monocyte production
tuberculin reaction
- positive response to the tuberculin test is mediate by Th1 T cells and not seen until 2-3 days after the initial injection
- if pt received BCG vaccine the test will be positive
