This article discusses newer cellular immunological and immunoregulatory events operative in the pathogenesis of "allergic alveolitis" (aa). An early increase in neutrophils and chemotactic factors followed by an influx of macrophages and lymphoid cells with ultimate production of granulomas have been demonstrated in the bronchoalveolar lavage (BAL) fluids of experimental animals and of man in aa. Transfer of specifically sensitized lymph node and spleen cells intraperitoneally followed by antigen challenge via the respiratory tract route has resulted in production of pulmonary lesions closely resembling those observed in human aa in several animal species. Activated alveolar macrophages and T-cells, local lymphokine production, and elevated immunoglobulin levels in BAL fluid have also been demonstrated repeatedly in experimental animal models of these diseases. High levels of interleukin-1 have also been demonstrated in aqueous extracts prepared from pulmonary granulomatous lesions. Other studies have indicated a role for macrophage-derived lipoxygenase products in production of experimental pulmonary granulomatous inflammation. Mononuclear cell pulmonary infiltrates have been inhibited by corticosteroids, the use of antimacrophage serum, neonatal thymectomy, cobra factor venom, and cyclosporin. A T suppressor factor and other suppressor factors from adherent cell populations have also been shown to dampen or modulate experimental granuloma formation. Appropriately sensitized animals which demonstrate chronic pulmonary granulomatous inflammation can also become "desensitized" following a series of antigen challenges. The desensitization produced is immunospecific and nontransferable with immune serum. Studies of bronchoalveolar lavage fluids in man have demonstrated a very high percentage of lymphocytes in BAL fluids. The percentage of suppressor cytotoxic T-cells is usually above 40% and CD4:CD8 ratios are reversed. Evidence also suggests that suppressor lymphocytic alveolitis is a chronic event in patients with aa. Immunogenetic studies of granulomatous pneumonitis resembling aa in different strains of mice have shown that certain high-responder strains develop intense granulomas after inoculation with killed bacille Calmette-Guérin (BCG), whereas other low-responder strains do not. The intensity of the pulmonary granuloma formation in this model has been shown to be a dominant and polygenic trait and to be linked to the immunoglobulin heavy chain locus (IgH). Strains that develop intense, chronic granulomatous inflammation have usually proved to be anergic, and the anergy also appears to be under genetic control.(ABSTRACT TRUNCATED AT 400 WORDS)