Lymphocyte subsets in hypersensitivity pneumonitis.

Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is the pulmonary manifestation of hypersensitivity to various categories of inhaled organic antigens. These include animal proteins from the faeces of pigeons or parakeets, or from duck and turkey feathers and antigens from various plant sources such as mouldy hay, sugar cane, bark and mushrooms. Certain drugs may also produce this reaction (1-3]. Sensitized individuals exposed to a large challenge develop an acute febrile illness, characterized by the abrupt onset of breathlessness, cough and chest pain within 4-6 h after exposure. This acute hypersensitivity reaction usually resolves spontaneously without sequelae after the offending agent has been withdrawn. Chronic insidious exposure to low levels of antigen, however, may lead to persistent attacks of breathlessness on exertion, with or without previous acute attacks, and diffuse interstitial lung disease, which in some cases will progress to interstitial fibrosis [4-5]. Histological studies of lung biopsies have shown that the inflammatory process affects the interstitium, alveolar space and terminal airways in an uneven distribution in the lung biopsy [6]. Epithelioid granulomas containing multinucleated histiocytes are often, but not invariably, present and are usually distributed around distal airways, in the interstitium and within alveolar spaces (6, 7]. The pathogenesis of hypersensitivity pneumonitis is not yet fully understood but immune mechanisms with or without amplification by immune complexes, lymphokines and other biological modifiers are thought to be involved [2]. Repeated antigen exposure in a susceptible host appears to stimulate chemotaxis and sensitize T-lymphocytes and macrophages, resulting in granuloma formation. Continued exposure finally results in the elaboration of growth factors that stimulate fibroblasts and result in collagen production [8]. Our understanding of the pathogenesis of this disease has been improved recently by widespread use of bronchoalveolar lavage (BAL). This provides a relatively non-invasive technique for sampling cells from peripheral lung tissue and, using monoclonal antibodies, cells recovered by BAL can be studied both from a phenotypic and functional point of view. The total number of cells recovered by BAL from patients with hypersensitivity pneumonitis is greatly increased, being three to five times that observed from controls