Hypersensitivity

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Hypersensitivity When Your Immune System
Overreacts !!!!!
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Definition
Non-specific coordinated response by
vascularized living tissue to injury
Functions Of Inflammation
_at_ Contain and isolate the injury
_at_ Destroy microorganisms/toxin
_at_ Prepare tissue for healing and repair
May be potentially harmful to the body
Involves cells and chemical mediators
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Inflammation
May be acute (short duration) or chronic (long
duration)
Depends on nature of the injury
In chronic inflammations, there are preliminary
and recurrent acute phases
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Inflammation
The interaction between effector molecule of the
immune system and the antigen produces this
localized inflammation
Some but not extensive tissue damage
When inflammation response is heightened and
damage is extensive HYPERSENSITIVITY
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Hypersensitivity
May develop in context of humoral or
cell-mediated immunity
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Inflammation
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Humoral Hypersensitivity
Antigen antibody complexes
Immediate hypersensitivity reactions
Symptoms manifest within minutes to hours
Classified into three types
Cell mediated Hypersensitivity
T-cell mediated
DTH (Delayed Type Hypersensitivity)
Useful for fighting pathogens
May however become excessive
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Gel Coombs Classification of Hypersensitivity
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Gel Coombs Classification of Hypersensitivity
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Type I
IgE-mediated
Due to allergens (antigens causing allergic
reactions)
Problem is that allergen induces IgE
IgE binds to surface of mast cells and basophils
(SENSITIZATION) (FIRST CONTACT)
Second exposure leads to cross linking IgE on
cell membrane (Degranulation of these cells)
Mediators released ? systemic or localized
reactions
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Why Do We Have IgE Response?

• Important in defence against parasites and large
  organisms where a much larger range of effector
  functions is required. Must also be rapid and
  all encompassing to provide protection against
  complex organisms such as parasites.

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Systemic Anaphylaxis
Resembles shock and is fatal
Within minutes of type I hypersensitivity
reactions
Blood pressure drops. Why?
Bronchioles constrict. Why?
May be due to bee, wasp or ant stings, drugs
(penicillin) or food (nuts)
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Mast Cell
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Localized Anaphylaxis
Limited to specific tissue or organ
Involve epithelial lining at site of allergen
entry
Atopy Tendency to develop localized anaphylactic
reactions
Hay fever most common (allergic rhinitis)
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GI Tract
Food allergens
Localized smooth muscle contractions ? vomiting
diarrhoea
Atopic
In atopic persons, allergens stimulate IgE
resulting in type I hypersensitivity reactions
Allergen enters by
_at_ Inhalation _at_ Ingestion
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Late Phase Reactions
As Type I reactions subside, late reactions arise
Eosinophils, basophils, monocytes an lymphocytes
are attracted by granular content
Eosinophils secrete inflammatory mediators
causing further damage
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Mediators Of Type I Hypersensitivity
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Treatment Of Allergies
Avoidance very difficult
Antihistamines most common for mild forms such
as hay fever
Corticosteroids essential for chronic
conditions such as Asthma
Cromoglycate stabilises mast cells
Sympathomimetics e.g. adrenalin in anaphylaxis
Desensitisation - low but increasing dose of
allergen to induce high affinity, mature IgG
rather than IgE competes for allergen
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Antibody-Mediated Cytotoxicity. Type II
Antibody-mediated destruction
Blood transfusion reactions are a classical
example
Antibody reacts with incompatible antigen on
transfused blood cell
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Type II Hypersensitivity Reactions
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Blood Transfusions
Group A Antigen A Group B Antigen B Group
AB Antigen A and B Group O Neither
Haemoglobin appears in urine (Haemoglobinurea)
Haemoglobin broken down to bilirubin (jaundice)
toxic (fever, chills and nausea)
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Haemolytic Disease Of The Newborn
Maternal IgG specific for foetal RBC crosses
placenta
Destroys foetal RBC Erythroblastosis Fetalis
Occurs in RH baby and RH- mother
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Immune Complex-Mediated Type III hypersensitivity
Reactions
Antigen antibody complexes are called immune
complexes (good)
Too much immune complexes (III hypersensitivity
reactions)
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TDTH-Mediated Type IV Hypersensitivity
TH and TC are activated
Interleukin 2, interferon gamma and tumour
necrosis factor alpha attract macrophages
Macrophages secrete lytic enzymes and cause
tissue destruction
e.g. Lung cavities seen in Mycobacterium
tuberculosis