IV. Clinical aspects of delayed hypersensitivity in lungs: pathophysiology of hypersensitivity disorders in clinics

Hypersensitivity pneumonitis (HP) is an immunologically mediated lung disease of inhaled antigens. HP is not a uniform disease but rather a clinical complex syndrome characterized by varying intensities of responsiveness to different organic antigens. The main aetiological agents include thermophilic bacteria, fungi, animal proteins, and chemical compounds. A combination of host and environmental factors should be considered as a requisite to developing this disease. Although the antigens differ widely, the clinical syndromes that results are very similar. HP occurs mainly in non-smokers, and clinically it may be in acute, subacute, or chronic forms. The diagnosis of HP requires a constellation of clinic, radiographic, physiologic, pathologic, and immunologic criteria. HP is characterized by a diffuse and predominantly mononuclear cell inflammation, a partly granulomatous, immune disorder of alveolar regions that often involves the small airway. A strong evidence supports that delayed cell-mediated hypersensitivity mechanisms play a role in pathogenesis of HP. Studies performed on lung cells have demonstrated that cells bearing suppressor/cytotoxic phenotype characterize the lymphocytic alveolitis in patients with hypersensitivity pneumonitis. And also recently evidence has been provided indicating that a prominent role of T-helper 1 cell-mediated hypersensitivity with an imbalance in T-lymphocyte subsets, although the deposit of immune complex may participate in an acute form of the disease as well as in the early phase of the chronic form.