Hypersensitivity IMMUNOLOGY

239 Pages·2016·14.68 MB·English

Ivo Boudakov, Ph.D.
Ver. 2016
Hypersensitivity
IMMUNOLOGY (BMIC550)
Learning Objectives FYI
 Topics and keywords to be discussed: Hypersensitivity I, II, III, and IV.
Description of Hypersensitivity type V reaction. Rhesus disease (Erythroblastosis
fetalis). Autoimmune hemolytic anemia. Idiopathic thrombocytopenia purpura. Cold
hem-agglutinin disease. Graves disease. Arthus Reaction. Serum sickness.
Glomerulonephritis. Rheumatoid arthritis. Systemic lupus erythematosus (SLE).
Tuberculin test. Contact sensitivity
131. List the Gell and Coomb’s classification of hypersensitivity
132. Describe the pathophysiologic mechanisms associated with Type I (IgE)-
mediated injury.
133. Compare and contrast the acute phase reaction with the late phase reaction
in anaphylaxis.
134. Explain the role of eosinophils in allergic and anaphylactic reaction.
135. Discuss the therapeutic modulation of Type I hypersensitivity. Explain the
proposed mechanism underlying “desensitization” (“allergy shots”).
136. Explain the principles underlying the RAST test and skin test. Explain how
they can be used as diagnostic tools.
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Learning Objectives FYI
136. List the categories of intervention for patients susceptible to Type I
hypersensitivities.
137. Explain the principle underlying desensitization therapy.
138. Describe allergic asthma.. Describe the bronchial wall changes that occur in
asthma.
139. Compare and contrast Type II and Type III hypersensitivity reactions.
140. Compare complement mediated cell lysis and antibody dependent cell
cytotoxicity.
141. Compare immunopathology of Goodpasture’s syndrome and SLE.
142. Compare and contrast drug induced Type I and Type II hypersensitivity
reactions.
143. Discuss the underlying reasons for the development of Erythroblastosis
fetalis.
144. Describe Type IV cell mediated hypersensitivity.
145. Recall the basis for, and examples of, contact hypersensitivity.
146. Explain the principle of, and immunology of a Mantoux test.
147. Describe granulomatous formation.
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Hypersensitivity
Under some circumstances immune system reaction causes

tissue and organ damage instead of protection
Such reactions are collectively known as hypersensitivity

Reaction could occur in two situations:

against environmental antigens

against self (autologous) antigens which is usually linked

to tolerance failure
Allergen is an antigen that causes harmful reaction and

technically it is linked with type I hypersensitivity.
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Basic characteristics of Hypersensitivity
Reaction is antigen specific

Reaction depends on the participation of antibodies or

lymphocytes
Prior exposure to an antigen is required (sensitization)

First contact with an antigen produces no detectable

reaction, but sensitizes the immune system
Secondary and any other re-exposure to the same antigen

elicit the hypersensitive reaction
Additional re-exposures to the same antigen may increase

or sometimes decrease the sensitivity of the reaction
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Hypersensitivity - Four (Five) Types
Type I (Immediate Hypersensitivity)

D
E
T
A IgE mediated reaction such as allergy or anaphylaxis

I
D
E
M Type II (Cytotoxic Hypersensitivity)


Y
D Antibody dependent (IgM or IgG) cytolytic reactions

O
B
I
T Type III (Immune Complex Hypersensitivity)

N
A
Immune complex reactions (mediated by IgM or IgG)

Type IV (Delayed Hypersensitivity -DTH)

cell mediated immunity, such as tuberculin test

Type V (Noncytotoxic or Stimulatory Hypersensitivity)

same underlining mechanism as type II hypersensitivity (IgG

or IgM) but instead of damage it alters tissue activation
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Type I – Immediate Hypersensitivity
Limited number of allergens when deposited in low doses on

mucosal epithelial cells or skin trigger mast cells activation
Allergens include

Pollens, trees, grass, and dust

Food allergens

Milk, eggs, fish, cereals, nuts

Insect bites, mite feces, dogs, cats

Reaction against drugs (penicillin) and other haptens,

mold spores, etc.
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Clinical Presentation of Type I Hypersensitivity
Wheel and flair – almost immediate

vasodilation with infiltrate presenting as
wheel and inflammation around
Atopic dermatitis (atopic

eczema) – itchiness which is not
caused by histamines
hence anti-histamines would not

help with eczema
1/5 infants (due to fragile skin)

vs. 1/50 adults develop eczema
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Clinical Presentation of Type I Hypersensitivity
Hives (urticaria) – itchiness

linked to histamine release
Individual lesions usually do

not last longer than 1-2 days
healthy lung inflamed
airway lung airway
Asthma – allergens act on the

tracheobronchial tree
Inflammation causes edema of

the airway wall
PENTAX Medical Company.
Hyper-secretion of mucus

causes airflow obstruction
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Clinical Presentation of Type I Hypersensitivity
Allergic rhinitis: (hay fever) –

acts on the mucus membranes of
the nose and eye
Congestion, itchiness, and

sneezing
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