Hypersensitivity pneumonitis (HP), also referred to as extrinsic allergic alveolitis, is characterized by non‐immunoglobulin E mediated inflammation of the parenchyma, alveoli, and terminal airways of the lung initiated by inhaled antigens in a susceptible host. Etiologic agents of HP are either organic high-molecular-weight compounds (e.g., bacteria, fungi, amoebae, plant and animal proteins) or inorganic low-molecular-weight haptens (e.g., isocyanates) and drugs (including amiodarone, nitrofurantoin, and minocycline). Six significant predictors have been identified that provide approximately 95% diagnostic accuracy. These six predictors are (1) exposure to a known offending allergen, (2) positive precipitating antibodies to the offending antigen, (3) recurrent episodes of symptoms, (4) inspiratory crackles on lung auscultation, (5) symptoms that occur 4‐8 hours after exposure, and (6) weight loss. HP is staged into acute, subacute, and chronic. In the acute stage, after direct exposure to the antigen, there are fever, chills, nonproductive cough, dyspnea, malaise, and myalgias, all of which resemble influenza. However, if obtained, a chest radiograph demonstrates nodular infiltrates, and pulmonary function testing is restrictive (unless the cause is avian, in which case, obstruction or obstruction with restriction is present). In the chronic stage, fever and chills are absent, but weight loss can occur. The immunologic response includes activated macrophages and CD8+ cytotoxic lymphocytes, and bronchoalveolar lavage fluid reveals marked lymphocytosis with a ratio of CD4+ to CD8+ cells of <1. Activated macrophages have increased expression of CD80/CD86, and T cells have increased expression of its counter-ligand, CD28, evidence for heightened antigen presentation.