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OBJECTIVE: T lymphocytes have a central regulatory role in the pathogenesis of asthma. The objective of this study was to characterize immunologically the activation stage of asthma and the functional profile of lymphocytes from induced sputum, with particular emphasis on gammadelta T cells. METHODS: Induced sputum was collected from 10 patients with acute exacerbation of asthma, and from healthy controls. The expression of activation markers on freshly isolated induced sputum lymphocytes and T-cell subsets was analyzed by double immunofluorescent staining and flow cytometry. Fas ligand (FasL) was determined by reverse transcriptase-polymerase chain reaction analysis. The phenotype of gammadelta T-cell subpopulations was tested by A13 and BB3 monoclonal antibodies. In this context, the functional profile of gammadelta T cells was tested in a chromium releasing test. RESULTS: A significantly decreased proportion of alphabeta T cells and an increased proportion of gammadelta T cells, CD56+ cells and CD8+ gammadelta T cells were found in asthma patients compared with healthy controls. In asthmatic patients, there is a significantly increased proportion of T cells expressing CD69 and CD25 antigen. After stimulation of gammadelta T cells, an increased expression of intracellular tumour necrosis factor-alpha, interleukin (IL)-4 and IL10 cytokines were found at higher levels than controls. Interferon-gamma was observed at similar levels in asthma patients and healthy controls. Freshly isolated T-cell receptor (TCR) gammadelta+ cells exhibited an increased percentage of FasL in our patient group. FasL mRNA was detected in TCR gammadelta+ cells before and after IL2 stimulation. TCR gammadelta+ cells were cytotoxic against the K562 cell line. This natural killer activity was mediated by the A13-positive subpopulation. CONCLUSION: The presence of cytokines producing gammadelta cells in induced sputum of asthmatic patients is consistent with regulatory activities. These cells display also cytotoxic function.

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Several reports have shown a defective Epstein‐Barr virus (EBV)‐specific suppressor T cell function in rheumatoid arthritis (RA), suggesting that EBV may have a role in the pathogenesis of RA. EBV‐specific T cell regulation was studied in 47 EBV‐immune RA patients and in 14 EBV‐immune control subjects by comparing the secretion of IgM into supernatants of 28‐day cultures of B cells alone and cocultures of B and autologous T cells. In control subjects, autologous T cells mediated a significant decrease in the secretion of IgM by B cells at 12 and 16 days of culture. Analysis of individual responses demonstrated the existence of 3 subgroups of RA patients: group I (18 patients) had a suppressor T cell function similar to that of controls; group II (21 patients) had a defective T cell function; group III (8 patients) was characterized by a “late help phenomenon.” Moreover, in RA group III, IgM secretion in cultures of B cells alone was lower than that seen in controls, RA group I, or RA group II. Differences in the duration or severity of the disease, or in the use of slow‐acting therapeutic agents, corticosteroids, and nonsteroidal antiinflammatory drugs could not account for these subdivisions. Thus, our study demonstrates that several immunoregulatory defects exist in subgroups of RA patients.