Immune complex-mediated hypersensitivity occurs when an antigen binds to an antibody within circulation, forming immune complexes that deposit in tissues. This causes inflammation and tissue damage. There are two types of antigens: exogenous like bacteria/viruses, and endogenous like self-components. When complexes activate complement or attract neutrophils, they cause inflammation and injury. Diseases include systemic lupus erythematosus, poststreptococcal glomerulonephritis, and the Arthus reaction, a localized skin necrosis from acute immune complex vasculitis.

2. Immune Complex-Mediated (Type III)
Hypersensitivity:
 Antigen combines with antibody within the
circulation (circulating immune complexes) , and
these are deposited.
 Antigen-antibody complexes produce tissue damage
by eliciting inflammation at sites of deposition.
 Two types of antigens cause immune complex-
mediated injury:
(1) exogenous antigens: such as foreign protein,
bacterium, or virus.(microbial proteins)
(2) endogenous antigens: individual can produce
antibody against self-components such as
nucleoproteins.

3. IMMUNE COMPLEXES
Antigen binds to IgG and
forms complex and
circulate through the blood
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.

5. Mechanism Of Tissue Injury
Immune complexes trigger inflammatory processes:
activate release
1) 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.

7.  Examples of Immune Complex-Mediated Diseases: [
diseases and antigens ]
 Systemic lupus erythematosus : DNA, and
nucleoproteins antigens.
 Polyarteritis nodosa : Hepatitis B virus surface antigen
 Poststreptococcal glomerulonephritis : Streptococcal cell
wall antigen.
 Acute glomerulonephritis : Bacterial antigens
(Treponema); parasite antigens (malaria, schistosomes);
and tumor antigens.
 Reactive arthritis : Bacterial antigens (Yersinia).

8.  Immune complex-mediated diseases can be:
generalized (systemic) ; or localized .
Systemic Immune Complex Disease:
Acute serum sickness: Once complexes are
deposited in tissues, they initiate an acute
inflammatory reaction (approximately 10 days after
antigen administration), clinical features such as
fever, urticaria, arthralgias, lymph node enlargement,
and proteinuria appear.
Local Immune Complex Disease :
Arthus reaction: a localized area of tissue
necrosis resulting from acute immune complex
vasculitis, usually elicited in skin.

12. ARTHUS REACTION
 Local inflammatory reaction with Necrosis
 Few hours after Ag inoculation
Inoculated Animal is previously immunized by same Ag
 immunized animal has titers of precipitating IgG Abs
 Arthus lesions evolve over a few hours and reach a
peak 4 to 10 hrs after injection
 When injection site develops visible edema with severe
hemorrhage occasionally followed by ulceration

13. General
hypersensitivity e.g.
serum toxicity.
Specific Reactions like
kidney lupus nephritis,
Joints rheumatoid
arthritis.

14. Anaphylaxis
Non human
proteins given
therapeutical
y bind to IgG.
These
complexes get
deposited in
the alveoli of
the lungs.
Inflammation
leads to
anaphylaxis.