Finally, the third step is the inflammatory reaction, during which the classical pathway is activated and macrophages and neutrophils are recruited to the affected tissues.

C3 can then be bound by CD35 on the surface of erythrocytes which delivers these immune complexes to phagocytes such as Kupffer cells and red pulp macrophages.

This is particularly noteworthy because systemic lupus erythematosus, a canonical type III hypersensitivity-driven autoimmune disease, has been associated with deficiency of certain components of the complement cascade, which promote persistence of the immune complexes.

These models support that Fc receptors play a dominant role in the response which can be augmented by the complement system via the anaphylatoxin C5a.

Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response.

[12] The relevance of the Gell and Coombs classification of allergic reactions is questioned in the modern-day understanding of allergy, and it has limited utility in clinical practice.