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Type III hypersensitivity

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Title: Type III hypersensitivity  
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Subject: Rheumatoid arthritis, Inflammation, List of diseases (H), Type I hypersensitivity, Hypersensitivity pneumonitis, Subacute bacterial endocarditis, Immune complex, Autoimmune disease, Systemic lupus erythematosus
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Type III hypersensitivity

Type III hypersensitivity
Classification and external resources
MeSH D007105

Type III hypersensitivity occurs when antigen-antibody complexes that are not adequately cleared by innate immune cells accumulate, giving rise to an inflammatory response and attraction of leukocytes.


Type III hypersensitivity occurs when there is an excess of antigen, leading to small immune complexes being formed that do not fix complement and are not cleared from the circulation. It is characterized by solvent antigens that are not bound to cell surfaces (which is the case in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different sizes form.[1] Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, a small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic.[2]

Such depositions in tissues often induce an inflammatory response,[3] and can cause damage wherever they precipitate. The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages).[4]

The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunlogic memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient (e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively) bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly associated conditions as a result of type III hypersensitivity responses[5]).

As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (fibrinoid necrosis). Often, immunofluorescence microscopy can be used to visualize the immune complexes [5]). Skin response to a hypersensitivity of this type is referred to as an Arthus reaction, and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of serum sickness.[4]


Some clinical examples:

Disease Target antigen Main effects
Systemic lupus erythematosus Nuclear antigens
Post-streptococcal glomerulonephritis Streptococcal cell wall antigens
  • Nephritis
Polyarteritis nodosa Hepatitis B virus surface antigen
Reactive arthritis Several bacterial antigens
  • Acute arthritis
Serum sickness Various
  • Arthritis
  • Vasculitis
  • Nephritis
Arthus reaction Various
  • Cutaneous vasculitis
Farmer's Lung Inhaled antigens (often mould or hay dust)
  • Alveolar inflammation
Henoch–Schönlein purpura Unknown, likely respiratory pathogen
Unless else specified in boxes, then ref is:[6]

Other examples are:


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