Hypersensitivities Flashcards
Type I hypersensitivity reactions are mediated by
IgE and results from the actions of mediators by mast cells
Type II hypersensitivity reactions are mediated by
Abs that bind tissue Ags and cause complement dependent tissue injury and disease
Type III hypersensitivity reactions are mediated by
Circulating Ag-Ab complexes which deposit in vessels and cause complement dependent injury in the vessel wall (vasculitis)
Type IV hypersensitivity reactions are mediated by
T cells and results from inflammation caused by cytokines produced by CD4+ Th1 and Th17 cells, macrophages, or killing of host cells by CD8+ CTLs
What happens in the initial allergen encounter in type I hypersensitivity reactions?
Th2 and IL-4
Adaptive immune response by B cells that mature into plasma cells to make IgE to that allergen
What unique property does IgE have?
It enters the circulation and is rapidly bound by FcRe (CD23) on mast cells in the tissues
What occurs during the subsequent allergen encounter during a type I hypersensitivity reaction?
Cross linking causes mast cell degranulation that releases vasoactive amines, cytokines/chemokines and lipids
What are the important mediators of type I hypersensitivity reactions?
Histamine, proteases, prostaglandins, leukotrienes and cytokines
What role does histamine play during type I hypersensitivity reactions?
The major amine that causes dilation of small vessels and increases vascular permeability
What role do proteases play during type I reactions?
May cause local tissue damage
What role do prostaglandins have during type I reactions?
Cause vascular dilation
What role do leukotrienes play in type I reactions?
Stimulate prolonged smooth muscle contraction
Describe immediate phase of type I reactions
Characterized by vasodilation, congestion and edema
Describe the late phase of type I reactions
Develops 2-24 hours later
Characterized by an inflammatory rich in eosinophils, neutrophils and T cells
What are the aims of allergen SIT?
To induce peripheral T cell tolerance to allergens
To increase the thresholds for mast cell and basophil activation by allergens
To decrease IgE mediated histamine released by mast cells