Type Iii Hypersensitivity:: Localised (Arthus Reaction) or

TYPE III HYPERSENSITIVITY :A hypersensitivity resulting from large quantities
of soluble antigen-antibody complexes passing between endothelial cells of the blood

vessels and becoming trapped on the surrounding basement membrane .
• Also known as immune complex hypersensitivity.
• The reaction may be-
localised ( arthus reaction) or
genralised as in -
- systemic lupus erythematosus, Arthus reaction.
- lupus nephritis.
- aspergillosis.
- polyarteritis.
- rheumatoid arthritis.
• The reaction may take 3-10 hours after exposure to the antigen (as in Arthus reaction).
• Mediated by soluble immune complexes.
• Mostly of IgG class, although IgM may also be involved.
• The antigen may be
exogenous (chronic bacterial, viral or parasitic infections),
endogenous (non-organ specific autoimmunity: e.g. SLE).
The antigen is soluble and not attached to the organ involved.

Type III-Mechanism of reaction
Step-1 Step-2
Large quantities of soluble antigen-
antibody complexes form in the blood and These antigen-antibody complexes lodge in the
are not completely removed by capillaries between the endothelial cells and the
basement membrane
macrophages .
Step-3
These antigen-antibody complexes activate the Step-4
classical complement pathway leading to The complement proteins and antigen-antibody
vasodilation complexes attract leukocytes to the area.
Step-5
The leukocytes discharge
their killing agents and
promote massive
inflammation. This can
lead to tissue death and
hemorrhage.
• Arthus Reaction: acute
Arthus Reaction antibody-mediated
hypersensitivity to soluble
Experimental antigens
model for
Immune Complex
disease • Comple
ment
activati
on
serum sickness
• A systemic type III reaction, can result from the injection of large
quantities of a poorly catabolized foreign antigen.
• frequently followed the administration of therapeutic horse
antiserum.
• Streptokinase (bacterial enzyme) .
• Antibiotics (penicillin or cephalosporin).
• occurs 7–10 days after the injection of horse serum.

• The clinical features
-chills,
-fever,
-rash,
-arthritis,
-glomerulonephritis.
• Urticaria is a prominent feature of the rash.
• Self-limiting disease
Course of serum sickness • Second dose of antigen follows the kinetics of a
secondary antibody response .
• Pathological immune-complex deposition
seen where antigen persists as in
-subacute bacterial endocarditis
-chronic viral hepatitis.

• The replicating pathogen is continuously
generating new antigen in the presence of a
persistent antibody response, with the
consequent formation of abundant immune
complexes.
• These are deposited within small blood
vessels, with consequent injury in many tissues
and organs, including the skin, kidneys, and
nerves.
Type III :- Rheumatoid arthritis
• Most often affecting women from 40
to 60 years .
• Many individuals with rheumatoid
arthritis produce a group of auto-
antibodies called rheumatoid factors
that are reactive with determinants
in the Fc region of IgG.
• Auto-antibodies bind to normal
circulating IgG, forming IgM-IgG
complexes that are deposited in the
joints.
• These immune complexes can
activate the complement cascade,
resulting in to chronic inflammation
of the joints.
• Also causes by type II mechanism.
Type III -Systemic Lupus Erythematosus
•Typically in women between 20 and 40 yrs.
•Female to male patients is 10:1.
• SLE is characterized by
-fever,
-weakness,
-arthritis,
-skin rashes,
-pleurisy,
-kidney dysfunction
• May produce autoantibodies to –
-DNA,
-histones,
-RBCs,
- platelets,
- leukocytes,
- clotting factors
•complement-mediated lysis of cells.
• .
• When immune complexes of auto-antibodies with various nuclear
antigens are deposited along the walls of small blood vessels, a type III
hypersensitive reaction develops.
• The complexes activate the complement system and generate
membrane-attack complexes and complement split products that
damage the wall of the blood vessel, resulting in vasculitis and
glomerulonephritis.
• As neutrophils attach to small blood vessels, the number of circulating
neutrophils declines (neutropenia) and various occlusions of the small
blood vessels develop (vasculitis).
• Laboratory diagnosis :- Antinuclear antibodies,directed against
doublestranded or single-stranded DNA, nucleoprotein, histones,
and nucleolar RNA.
Autoimmune Glomerulo-nephritis
Common Locations of Vascular Involvement
Hypersensitivity Pneumonitis Syndromes and
Associated Antigens
Farmer’s lung thermophilic actinomycetes
Malt worker’s lung Aspergillus spores
Pigeon fancier’s disease avian proteins
Cheese washer’s lung Penicillium spores
Furrier’s lung fox fur
Laboratory technician’s lung rat urine proteins

Type IV (delayed) Hypersensitivity-
A hypersensitivity resulting from cell-mediated immunity
(cytotoxic T-lymphocytes and cytokines) causing harm to the body
• Used to describe the signs and symptoms associated

with a cell mediated immune response.
• Results from reactions involving T lymphocytes.
• Koch reaction caused by injection of
tuberculoprotein (PPD test) intradermally resulting in
an area of induration of 5 mm or more in diameter
and surrounded by erythema within 48 hours is a
positive.
Type IV (delayed) Hypersensitivity
• Characteristics of this phenomenon are:
– Delayed, taking 12 hours to develop.
– Causes accumulation of lymphs and macrophages.
– Reaction is not mediated by histamine.
– Antibodies are not involved in the reaction.
• Cell mediated reactions in certain circumstances are wholly
damaging and may be seen in the following conditions:
– Drug allergy and allergic response to insect bites and stings.
– Contact dermatitis.
– Rejection of grafts.
– Autoimmune disease.
Delayed-type hypersensitivity is mediated by T cells
(Type IV hypersensitivity)
& mango sap

Delayed-type hypersensitivity (DTH)
(e.g., tuberculin skin test)
TH1 from a previous

immunization
(memory)
Chemical Mediators of DTH
A positive tuberculin skin test is a

DTH reaction
Before the distinction

between TH1 and TH2
(circa 1990), there was
TH cell and TDTH.
TH is now TH2 and TDTH is
now TH1
DTH as a result of a contact-sensitizing agent*
Contact Dermatitis Can be caused by poison ivy and mango sap
*a contact-sensitizing agent is usually a small molecule

that penetrates the skin then binds to self-proteins,
making the protein “look” foreign
TYPE 4 CLINICAL MANIFESTATIONS:
CONTACT DERMATITIS
• LOCALIZED TO THE SKIN

• MAXIMUM RESPONSE 24-
48 HOURS AFTER
EXPOSURE
• SYMPTOMS ARE
ERYTHEMA AND Poison Ivy
INDURATION -
SOMETIMES BLISTERING
EXAMPLES OF TYPE 4 HYPERSENSITIVITY:
CONTACT DERMATITIS
• TRIGGERED BY CERTAIN
MATERIALS
– METALS (e.g.: NICKEL IN Rubber in Brassiere
JEWELRY, WATCHES)
– CLOTHING
– RUBBER (e.g.: ELASTIC,
Nickel in Watch Strap
GLOVES, CONDOMS)
– LEATHER
– COSMETICS
– PLANTS (e.g.: POISON IVY)
Patch Testing
Hypersensitivity

Type Iii Hypersensitivity:: Localised (Arthus Reaction) or

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TYPE III HYPERSENSITIVITY :A hypersensitivity resulting from large quantities

of soluble antigen-antibody complexes passing between endothelial cells of the blood

The antigen is soluble and not attached to the organ involved.

• occurs 7–10 days after the injection of horse serum.

-chronic viral hepatitis.

Farmer’s lung thermophilic actinomycetes

Malt worker’s lung Aspergillus spores

Pigeon fancier’s disease avian proteins

Cheese washer’s lung Penicillium spores

Furrier’s lung fox fur

Laboratory technician’s lung rat urine proteins

• Used to describe the signs and symptoms associated

& mango sap

TH1 from a previous

A positive tuberculin skin test is a

Before the distinction

Contact Dermatitis Can be caused by poison ivy and mango sap

*a contact-sensitizing agent is usually a small molecule

• LOCALIZED TO THE SKIN

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