What is the Mechanism of Type III Hyper Sensitivity?

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When Ag-Ab complexes are not properly removed from the system, they get deposited on the surrounding tissue, and trigger a variety of inflammation processes.

The activation of complement system is one of them. The C3a and C5a fragments of activated components of the complement system are anaphylactic in nature and initiate release of vasoactive amines such as histamine serotonin etc. from mast cells and basophils ensuing inflammation.

Usually activity of complement system helps in the removal of foreign bodies through lysis or phagocytosis, but in Type III Hyper sensitive reactions, the cells that are removed by this process are normal cells to which left out Ag- Ab complexes are attached resulting in necrosis (destruction of cells).

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Through chemotactic action of C5a, Polymorphonuclear cells (PMNs) also reach the site of inflammation and attempt to ingest Ab – Ag complexes.

Since the complexes are trapped in the tissue they fail to ingest them. Therefore they release their lytic enzymes in the vicinity of the reaction, ensuing lysis of host cells around the reaction site.

In normal conditions lysosomal secretions released in to the blood or tissue are rapidly neutralized by certain inhibitor enzymes. But in Type III Hyper sensitivity reaction, the phagocytes gather close to the tissue trapped immune complexes through Fc binding, hence serum inhibitors are excluded and destruction of tissues is continued by the activity of lytic enzymes.

In addition to complement system platelets also interact with the left out immune complexes through their receptors for Fc region of Abs, release their secretions ensuing microthrombus formation, followed by an increase in vascular permeability.

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Since the platelets are a rich source for growth factors, their release may result in abnormal proliferation of immune cells also in the site of reaction. The increased vascular permeability allows immune complexes deposition on tissues.

The turbulence in blood flow and high blood pressure will also induce deposition of immune complexes leading to pathological conditions like arthus reaction, glomerulonephritis etc.

The intensity of reactions generally depends upon the concentration of antigen to that of Ab and the reactions may be local or systemic like other hyper sensitivity reactions.

Examples for Type III Hyper Sensitivity

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(1) Arthus Reaction (A Local Type III Hyper Sensitivity):-

It was named after the scientist who first observed it in rabbits. It is a local reaction that has been formed on the skin after intra dermal injection of antigen.

Binding of an antigen with circulating antibodies results in this kind of reaction. Symptoms of the reaction may appear in 2 to 8 hours after the injection of antigens and persists for about 12 to 24 hours.

The reaction starts as an erythematosus edema due to local hemorrhage and thrombosis in average limits. The reactions begin with marginalization (attachment of the cells to the wall of blood vessel) and migration of neutrophils through the walls of blood capillaries.

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Infiltration of the neutrophils continue till the reaction has reached to maximal intensity (for about 6-8hours). As the reaction progresses, destruction of walls of blood vessels take place, resulting in edema and hemorrhage. This vascular destruction is associated with platelet aggregation and thrombosis.

The antigen injected into the body diffuses away from the site of injection through tissue spaces and crosses the walls of small blood vessels, enters into the circulation and encounters the Abs.

As a result, immune complex is generated and deposited in between and beneath the epithelial cells leading to the initiation of Type III Hyper sensitivity reactions.

(2) Serum Sickness (Systemic Hyper sensitivity reaction): –

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It is a systemic hyper sensitive reaction. When antigens are administered intravenously to animals with a high level of circulating Abs, development of immune complexes takes place in circulation.

The larger complexes are removed by phagocytosis, but small complexes formed in antigen excess escape phagocytosis. These escaped small complexes induce complement fixation, platelet aggregation and release of vasoactive amines and thus alter the properties of vascular endothelium.

When the escaped immune complexes adhere to the cells of certain vital parts such as glomeruli, choroid plexus, vascular filters etc., they get damaged by systemic hyper sensitivity reaction.

(3) Farmers lung: –

Repeated inhalation of certain antigens such as asbestos, pesticides etc., leads to the formation and deposition of immune complexes on the surface of lungs in pre sensitized persons. This leads to considerable destruction of alveoli through Type III hyper sensitivity.

As the antibodies formed for the antigens are IgG type, the reactions are not of Type I hyper sensitivity reactions.

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