Von Pirquet first described serum sickness, the prototype of Immune Complex
disease in 1925. Any food protein or peptide entering the circulation in sufficient
quantity can produce symptom patterns resembling serum sickness. If antigens
make it into the blood stream, they combine with circulating antibodies to
produce circulating immune complexes (CICs).
Immune cells interact with CICs, triggering immune reactions with the release
of symptom-producing mediators. Serum sickness manifests as a systemic illness,
typically evolving over a period of 7-10 days. Manifestations include general
malaise, fever, flushing, sweating, hives, swelling, bruising, aching in joints
and muscles, progressing in the worst case to inflammatory disease in target
organs with protein in the urine from kidney damage.
Food-enriched blood, coming from the gastrointestinal tract, goes through the
liver where most immune-complexes are removed. If circulating complexes pass the
liver filter, they may cause disturbances in many organs. The other path of
absorption of molecules from the digestive tract is through lymphatic drainage.
The lymph channels flow together to form the thoracic duct, a flimsy vessel
which drains its contents into the subclavian vein. This pathway may direct
antigenic molecules directly to the lungs where food antigens may excite
asthmatic attacks, bronchitis, or more serious and enigmatic inflammatory lung
diseases. The combination of antibody with antigen in the blood stream is a
circulating immune complex (CIC).
CICs have the general form of: Antigen---Antibody
CICs may simply be removed from the circulation by macrophages or they may
trigger a cascade of events which lead to multiple symptoms, and possibly tissue
CICs ---> Mediator release ---> Symptoms
Mediators + Immune cells ---> Inflammation
CIC's activate complement, a circulating system of 25
proteins which interact to produce a variety of defensive molecular weapons.
CIC's may not cause tissue injury unless access to tissue spaces is increased by
leakiness of blood vessels, allowing influx of CIC's and cells. CIC's may not
cause tissue injury unless vascular permeability is increased - allowing influx
of CIC's and cells. The complement system modulates and amplifies the biological
effects of CIC's.
The main function of the complement cascade is to assemble a drilling rig
made of proteins attached to a cell wall and then to drill holes in the cell
wall, allowing its contents to flow out. Complement intends to punch enough
holes in a cell to kill it. If the attacked cell is a bacteria threatening to
invade your private parts, your are happy with complement activity. If these
drilling rigs are punching holes in your own cell walls, you will not be so
happy. This sort of complement misadventure does occur. Like most immune attack
systems, complement has go and stop mechanisms.
We can say that complement system modulates and amplifies the biological
effects of CIC's. Once activated the complement cascades through a series of
changes, producing powerful effects including anaphylaxis and blood cell damage.
At the same time, certain complement products are essential to clear CIC's and
to stop the cascade of cell damage. Individuals with deficiencies of complement
proteins are at greater risk of developing immune-complex disease.
CIC's leave capillaries to trigger inflammatory events in target tissues. A
classic model of complex-induced pathology is the Arthus reaction which appears
3-6 hours after antigen challenge and involves large insoluble (Type 3)
complexes with complement (C3b) passing through vessel walls to excite
inflammatory responses in target tissues. The Arthrus reaction can be prevented
by depleting C3 with Cobra venom
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