Hypersensitivity type 3

Larger complexes activate complement in the blood and are phagocytosed by

macrophages.

These moderate complexes are deposited

in the basement membranes of blood vessels and tissues.

Here they cause inflammation of target tissue/organ

through the attraction of leucocytes leading to

anaphylactic shock.

Mechanism Of Tissue Injury Immune complexes trigger inflammatory processes:

activate release1) Immune complexes the complement anaphylatoxins C3a, C5a

stimulate release degranulation of basophiles and mast cells histamine

Histamine vascular permeability and help deposition of immune complexes

2) Neutrophils are attracted to the site by immune complexes and release lysosomal enzymes which damage tissues and intensify the inflammation process.

Attributes

• Pathogenic mechanism of many disease causing microbes

• Reaction takes 3- 10 hours after exposure.• Mostly IgG involved and rarely IgM.

General hypersensitiv

ity e.g. serum

toxicity.

Specific Reactions like kidney lupus

nephritis,Joints

rheumatoid arthritis.

Examples

• Serum sickness• Arthus reaction• Rheumatoid arthritis

Anaphylaxis

Non human

proteins given

therapeuticaly bind

to IgG.

These complexe

s get deposited

in the alveoli of the lungs.

Inflammation leads

to anaphylax

is.

Risk Factors

• There are some gender differences between diseases of type II hypersensitivity. Some diseases are more common in women such as rheumatoid arthritis.

How is Hypersensitivity reaction – Type III Treated?

• Treatment options, either given alone or in combination, include the following:

• steroids: these drugs include dexamethasone. Depending on the diseases, steroid could become a long-term medication. In such cases, long term use will need medical supervision for monitoring of potential side effects.

• interferons, cyclosporin.