Exam 2- Type I Hypersensitivity Flashcards
what is an inflammatory response that causes extensive damage to the host’s tissues, even death, called?
hypersensitivity or allergy
IgE-mediated type I hypersensitivity (immediate hypersensitivity) is caused by coming into contact with an antigen against which the host has ________________________
pre-existing IgE antibodies
where are high affinity Fc-epsilon-RI receptors found?
mast cells, basophils, and eosinophils
true/false: allergens are typically presented to the immune system as high doses
false: very low doses
which Th cell response is required to induce type I hypersensitivity reactions?
Th2
what do mast cell granules do?
potent mediators immediate hypersensitivity reactions
how are mast cells, basophils, and eosinophils activated once the IgE molecule is bound?
cross-linking of the Fc-epsilon-RI receptors
what are the primary and secondary mediators?
primary: pre-formed and stored in granules, immediate hypersensitivity
secondary: synthesized after or released by enzymatic breakdown of cell membrane phospholipids during degranulation process
is histamine short-lived or long-lived?
short-lived
is the genetic predisposition to develop Type I hypersensitivity multigenic?
yes
true/false: the majority of IgE in the body is present in blood
false
true/false: mast cells of non-allergic individuals have IgE antibodies bound to the surface of their mast cells
true
what are the phases of type I hypersensitivity?
sensitization phase
activation phase
effector phase
what does the “wheal and flare reaction” show?
locally dilated blood vessels engorged with red blood cells
what does the late phase reaction of type I hypersensitivity consist of?
accumulation of inflammatory leukocytes
what inhibits the late phase of type I hypersensitivity reactions (rich in eosinophils)?
corticosteroids, not antihistamines
what is allergic rhinitis?
airborne antigens react with IgE-sensitized mast cells in nasal passages and conjunctiva
what is system anaphylaxis or anaphylactic shock caused by?
systemic release vasoactive mediators (mainly histamine and leukotrienes)