Rhinitis is a heterogeneous condition that has been associated with inflammatory responses as
in allergic rhinitis but can also occur in the absence of inflammation such as in so-called
‘idiopathic’ (previously ‘vasomotor’) rhinitis. Allergic rhinitis affects approximately 1 in 4 of
the population of westernised countries and is characterized by typical symptoms of nasal
itching, sneezing, watery discharge and congestion. The intention of this review is to
illustrate key concepts of the pathogenesis of rhinitis. Imbalance in innate and adaptive
immunity together with environmental factors is likely to play major roles. In allergic rhinitis,
initial allergen exposure and sensitization involves antigen presenting cells, T and B
lymphocytes and results in the generation of allergen-specific T cells and allergen specific
IgE antibodies. On re-exposure to relevant allergens crosslinking of IgE on mast cells results
in the release of mediators of hypersensitivity such as histamine and immediate nasal
symptoms. Within hours, there is an infiltration by inflammatory cells, particularly Th2 T
lymphocytes, eosinophils and basophils into nasal mucosal tissue that results in the late-phase
allergic response. Evidence for nasal priming and whether or not remodelling may be a
feature of allergic rhinitis will be reviewed. The occurrence of so-called ‘local’ allergic
rhinitis in the absence of systemic IgE will be discussed. Non-allergic (non-IgE mediated)
rhinitis will be considered in the context of inflammatory and non-inflammatory disorders.