gammadelta T cell populations are known to expand in response to intracellular bacterial infectious agents regardless of previous priming. We have shown previously that soluble factor(s) produced by Mycobacterium-stimulated monocytes activate cord blood gammadelta T cells to proliferate. In this study, we investigated whether cytokines produced by monocytes are responsible for gammadelta T cell activation in vitro: interleukin (IL)-1beta, IL-6, IL-8, IL-12, tumor necrosis factor (TNF)-alpha and granulocyte/macrophage colony-stimulating factor were examined. Recombinant human IL-12 stimulated gammadelta T cells, but not alphabeta T cells in peripheral blood mononuclear cells, to express CD25 on their surfaces, and to expand in number in vitro. IL-12-primed gammadelta T cell numbers increased to a greater extent in the culture to which exogenous IL-2 (5 U/ml) was added. Anti-TNF-alpha monoclonal antibody inhibited IL-12-induced up-regulation of CD25 on gammadelta T cells, suggesting that endogenous TNF-alpha may play a role in IL-12-induced activation of gammadelta T cells. Recombinant TNF-alpha synergistically augmented IL-12-induced activation of gammadelta T cells. Furthermore, IL-12 up-regulated TNF receptors on gammadelta T cells in vitro: TNF-alpha binding to its receptor induced CD25 expression on the gammadelta T cells in an autocrine or paracrine fashion, or perhaps both. It also became evident that both IL-12 and TNF-alpha were produced by mycobacterial lysate-stimulated monocytes. Taken together, these results suggest that upon confrontation with mycobacterial organisms, gammadelta T cells can be quickly and antigen-nonspecifically activated by soluble factors including IL-12 and TNF-alpha, both of which are produced by mononuclear phagocytes in response to mycobacterial organisms.

We studied summer-type hypersensitivity pneumonitis believed to be induced by Cryptococcus albidus in the home environments of the patients. All patients had antibodies that were reactive to Cryptococcus neoformans and Trichosporon cutaneum in sera and bronchoalveolar lavage (BAL) fluids. Cryptococcus albidus strains were isolated from 62.5% of the patient home environments. Trichosporon cutaneum was found in none of the patient homes. To study local antibody production in the lung, we cultured BAL cells to measure anti-C. neoformans and anti-T. cutaneum antibodies in the culture supernatants by the ELISA method. IgG, IgA, and IgM anti-Cryptococcus and anti-Trichosporon antibodies were found in all culture supernatants. A significant correlation was observed in antibody binding activity between Cryptococcus and Trichosporon antigen. However, the amount of IgA and IgM antibody bound to C. neoformans was significantly higher than was bound to T. cutaneum. Most anti-Cryptococcus and anti-Trichosporon antibody was absorbed by C. albidus. Our results suggest that C. albidus may be an etiologic agent in most of the cases we studied, and that IgA and IgM antibody in BAL fluid may be secreted by plasma cells in the lung.

Summary Clinical and immunological studies were made in forty‐two patients diagnosed as suffering from hypersensitivity pneumonitis at Osaka Prefectural Habikino Hospital between 1973 and 1977. All the sera from forty‐one patients tested had high litres of antibody against Cryptococcus neoformans in indirect fluorescent antibody tests, and twelve also had precipitins against Cryptococcus neoformans polysaccharide. Only about 10% of control sera from patients with otherlung diseases had low titresof antibody against Cryptococcus neoformans. Antibody against Cryptococcus neoformans was also found frequently in the sera of asymptomatic members of the families of the patients. A possible relationship of Cryptococcus neoformans to hypersensitivity pneumonitis is suggested.

Sixty-six patients, diagnosed as Japanese summer-type hypersensitivity pneumonitis at Osaka Prefectural Habikino hospital between 1973 and 1980, were studied. The diagnosis was based on the clinical features and summer-seasonal nature of the disease. The presence of an aetiological agent within patients" home environment was suggested by the recurrence of acute symptoms of high fever, cough and dyspnoea 5-8 hr after coming home from hospital, and by spontaneous improvement on leaving home, immunological studies revealed the presence of -dnU-Cryptoeoceus antibody in sixty-four of sixty-five patients' sera, by indirect immunofluorescence against Cryptococcus neoformans. Precipitating antibody against culture supernatant protein-antigen of Cr. n<'o/()rmam was detected in more than 80% of sera obtained from patients during the active stage of the disease. The positive result on inhalation provocation-challenge, using culture supernatant protein-antigen, suggested that Cr. neoformans or antigenically related Cryptococcus species may cause Japanese summer-type hypersensitivity pneumonitis. Recent studies reveal that patients with HP have been increasing during the past 10 years in Japan. Hypersensitivity pneumonitis in Japan, including our cases, was

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