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Hypersensitivity

Reactions

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Type I
Hypersensitivity
Immunologic Sensitization

Immunologic sensitization

Re-exposure to sensitizing protein

Manifestations of allergy
Signs and symptoms in target organs
Skin, GI, Lungs
Type I Hypersensitivity
• Type I (immediate type) reactions include: asthma, hay
fever, food allergy
• Also referred to as atopy
• Triggered within minutes of exposure to a variety of
environmental antigens e.g. pollen, house dust mite
• Strong genetic link
• Caused by an overproduction of IgE
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Initial
Respone
&
Late Phase
Reaction
Mast cell
activation
affects many
tissues
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Figure 10-12

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Type II
Hypersensitivity
Type II hypersensitivity (IgG-
mediated anti-cell-associated antigen
response) is rare
Immune response to certain drugs (e.g.,
penicillin) where drug binds to cell
surface and antibody cause removal of
the cells (usually by macrophages).
Figure 6-14 Schematic illustration of the three major mechanisms of antibody-mediated injury. A, Opsonization of cells by antibodies and complement components and
ingestion by phagocytes. B, Inflammation induced by antibody binding to Fc receptors of leukocytes and by complement breakdown products. C, Antireceptor antibodies
disturb the normal function of receptors. In these examples, antibodies against the thyroid stimulating hormone (TSH) receptor activate thyroid cells in Graves disease,
and acetylcholine (ACh) receptor antibodies impair neuromuscular transmission in myasthenia gravis.

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 15 November 2005 09:36 AM)
© 2005 Elsevier
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Type II Antibody- dependent cytotoxicity

• Complement membrane attack complex, cell lysis


– Hemolytic transfusion reaction ABO incompatibility
– Hemolytic disease of newborn ( ABO, Rh)
– Autoimmune reaction ( Hemolytic anemia )
• Ab dependent cell mediated cytotoxicity (ADCC)
target cell coated with IgG
phagocyte (PMN, macrophage, NK cell) Fc receptor Ig G lysis of the target cell
requires contact

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• Ab depentdent cellular dysfunction

Ab against cell surface receptors impair or stimulate cell


function without causing cell injury or inflammation
- Myasthenia gravis
- Graves disease

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Type III
Hypersensitivity
Type III Immune Complex Mediated Hypersensitivity

• Ag-Ab immune complex deposit in blood vessel wall, microthrobi, endothelial damage,
inflammatory process, complement activation, phagocyte chemotaxis , accumulation of
neutrophils, damage basement membrane
• Local type (Arthus reaction): local tissue necrosis from acute immune vasculitis

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• Systemic type :

• Ag-Ab immune complexes form in the circulation

• deposition of immune complexes in various tissues: kidney, joints,


skin, small vessels

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Figure 10-29

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Type III hypersensitivity

Arthus Reaction: acute antibody-mediated


hypersensitivity to soluble antigens

Complement
activation

Type I, II, III are Immediate-type


hypersensitivities
Figure 10-31

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Type IV
Hypersensitivity
Type IV Mechanism
• APC resident in the skin
process antigen and migrate
to regional lymph nodes
where they activate T cells
• Sensitised T cells migrate
back to the the skin where
they produce cytokines which
attract macrophages which
cause tissue damage

© Dr JG Lawrenson 2001
Th1 derived
cytokines and
chemokines
direct Type IV
reactions
Type IV Cell- Mediated, Delayed- type hypersensitivity
• T cell
• against intracellular bacteria (TB, leprosy), fungal, viral, parasite, transplantation
• TB (tuberculosis) : activated macrophages with modified epithelial-like appearance (epitheloid
cells), granuloma = chronic granulomatous inflammation
• sentitized T cell directly kill cells
• Tc cell (cytotoxic T lymphocyte): effector cells

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Types of Immune Hypersensitivity Reactions
Types of Immune Hypersensitivity Reactions

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