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hypersensitivity, insert the photo with the four stages of type I…
hypersensitivity
Type IV. Cell-mediated (delayed)
hypersensitivity
causes
autoimmunity
environmental antigens
Mechanism
using T cells
T cells produce cytokines to
cause inflammation and recruit more lymphocytes
using B cells
produce NK cells
disease
contact dermatitis
eg when you wear a watch for long periods of time
therapy
corticosteroids
TNF antagonists
anti B7 (to inhibit T cell responses)
Type III. Immune complex-mediated hypersensitivity
what:
binding directly to their target antigens on the surface of cells and in the extracellular matrix
the antibody binding to the target is deposited at the site of infection
The main difference is that the antigens in t
ype II dont move round,
the antibodies bound to them to cause symptoms at that location, but in
type III the antigen antibody complex is formed first then it moves around to deposit the complex
therapy for type II and III
corticosteroids
IV IgG from healthy donors
anti CD20 (depletion of B cells)
anti CD40 (inhibit pdtn of anitbodies)
anti CD40L (inhibit pdtn of anitbodies)
disease
Arthurs reaction
(not arthurs)
serum sickness
Type II. IgG and IgM (antibody)-mediated hypersensitivity
what:
by forming immune complexes that deposit mainly in blood vessels
the complex of the antibody surrounding the cell travels throughout the cell
disease
graves
Haemolytic disease of newborn
Myasthenia gravis
types of hypersensitivity overview
Type I. Immediate hypersensitivity (IgE)
caused by
foreign antigens
self antigens
stages
Sensitization
Activation of Mast cells and Secretion of Mediators
Late-phase Reaction
biological mediators in
mast cell degranulation
Histamine
Dilation of small blood vessels
Increase vascular permeability
Protease
tryptase
cleaves fibrinogen and
activates collagenase
damage to local tissues
chymase
degradation of epidermal basement
membrane and stimulate mucus secretion
Lipid mediators
Prostaglandin
Vascular dilation, Chemotaxis, attracts neutrophils
Leukotrienes
binds to smooth muscle cells causing prolonged smooth muscle contraction
platelet activating factor (PAF)
binds to smooth muscle cells causing bronchoconstriction
cytokines and chemokines
TNF- alpha
activate endothelial cells
to cause leakage
IL-4 and IL-13
Th2 response
IL-5:
activates eosinophils
clinical symptoms
systemic
anaphylaxis
acute
urticaria
allergic
rhinitis
food
allergy
Diagnosis
Total IgE (>100 IU/ml)
Specific IgE
Serum Tryptase (anaphylaxis)
therapy includes
epinephrine
corticosteroids
antihistamines
(basically non-inflammatory drugs)
insert the photo with the four stages of type I hypersensitivirt