Hypersensitivity Disorder Flashcards
Describe type I hypersensitivity reaction.
IgE mediated from mast cells. contribute to anaphylactic reaction
Describe type II hypersensitivity.
Mediated by Ab that bind tissue Ag and activate complement to degrade specific tissue. Causing tissue injury/disease.
Describe Type III hypersensitivity.
Form from Ab-Ag complex that form in the blood, and settle in the vascular lining. Causing vasculitis
Describe a Type IV hypersensitivity reaction.
T cell mediated from inflammation by cytokines.
Ultimately from Th17, Th1 cells or killing CTL
What is the mechanism of a type I allergic reaction?
- Mast cells cross-link to IgE bound on Ag.
- Mast cells release pre-formed cytokines, vasoactive amines
- Also attract neutrophils/eosinophils
Where do mast cells bind to their high affinity IgE molecules?
Fc(epsilon)RI
What occurs in the immediate phase reaction of type I reactions?
Vascular and smooth muscles react within minutes.
1. Generally vasodilation, bronchoconstriction, edema, congestion
What occurs in the laste phase of type I allergic reactions?
Inflammation caused by eosinophils, neutrophils and T cells
What is the role of leukotrienes?
Prolonged smooth muscle contraction (bronchi) increase vascular permeability
What is the role of proteases in type I allergic reaction?
Tissue damage
What is the role of vasoactive amines in a type I allergic reaction?
Cause vasodilation, smooth muscle contraction (bronchi)
What is the role of cytokine secretion during type I allergic reaction?
Cause inflammation and leukocyte recruitment for late phase response
What are the effector mechanisms of type II allergic reaction?
- Abs opsonize which activate complement and phagocytosis via CR1/FcR affinity for C3b
- C3a/C5a recruit leukocytes
- Ab can stimulate/inhibit a glands receptor
What disease can be caused by Ab binding during a type II allergic reaction?
Ab bind with TSHreceptor, causing hyperthyroidism (Grave’s disease)
What binding can be inhibited in a type II allergic reaction by the antibody?
Inhibition of Ach binding to receptor causing myasthenia gravis