Adaptive immunity, specifically the Th2-mediated immune response, plays a crucial role in allergies and asthma.

IgE binds to mast cells and basophils, triggering the release of inflammatory mediators such as histamine and leukotrienes.

Mast cells are the primary effector cells in immediate hypersensitivity reactions, releasing inflammatory mediators upon allergen binding to IgE.

Th2 cells promote inflammation and IgE production, contributing to the allergic response.

Interleukin-5 (IL-5) is the primary cytokine responsible for eosinophil recruitment and activation in allergic inflammation.

Antihistamines work by blocking the binding of IgE to mast cells, preventing the release of inflammatory mediators.

Allergic asthma is characterized by an allergic response to specific allergens, such as pollen, dust mites, or pet dander.

Inhaled corticosteroids primarily work by reducing airway inflammation in asthma treatment.

Airway smooth muscle cells are primarily responsible for airway remodeling in asthma, leading to increased airway responsiveness and airflow obstruction.

Leukotriene modifiers work by inhibiting the release of inflammatory mediators, such as leukotrienes, from activated cells.

Exercise-induced asthma is triggered by physical exertion and is characterized by airway narrowing and shortness of breath during or after exercise.

Bronchodilators primarily work by relaxing airway smooth muscle, relieving bronchoconstriction, and improving airflow.

Occupational asthma is caused by exposure to specific occupational irritants or allergens, such as chemicals, dust, or fumes.

Cromolyn sodium works by preventing the binding of IgE to mast cells, stabilizing mast cells, and inhibiting the release of inflammatory mediators.

Non-allergic asthma is characterized by chronic airway inflammation and airflow obstruction, but it is not triggered by specific allergens.