Type I hypersensitivity reaction is a rapid allergic response mediated by IgE antibodies.
This immediate hypersensitivity occurs within minutes of allergen exposure and can manifest as hives, asthma,
rhinitis, or severe anaphylaxis. Understanding this mechanism is crucial for managing allergic diseases.
The sensitization phase occurs during the first exposure to an allergen.
Antigen-presenting cells process the allergen and activate T-helper cells, which then stimulate B cells
to differentiate into plasma cells. These plasma cells produce IgE antibodies that bind to mast cells
and basophils, sensitizing the body for future allergic reactions.
During the effector phase, upon second exposure to the same allergen,
the allergen binds to IgE antibodies already attached to mast cells. The critical step is
cross-linking of adjacent IgE antibodies by the allergen, which triggers immediate mast cell
activation and degranulation, leading to the rapid release of inflammatory mediators.
Mast cell degranulation releases both preformed and newly synthesized mediators.
Preformed mediators like histamine cause immediate vasodilation and itching, while newly synthesized
mediators like leukotrienes cause bronchoconstriction. These mediators collectively produce the
characteristic symptoms of allergic reactions including increased vascular permeability and smooth muscle contraction.
Type I hypersensitivity manifests with various symptoms ranging from mild to life-threatening.
Mild symptoms include urticaria, allergic rhinitis, and conjunctivitis. Moderate symptoms involve allergic asthma
and gastrointestinal reactions. Severe anaphylaxis can cause systemic vasodilation and cardiovascular collapse,
requiring immediate treatment with epinephrine. Understanding these manifestations is crucial for proper diagnosis and management.