Local Expansion of Allergen-Specific CD30+Th2-Type γδ T Cells in Bronchial Asthma
1995; BioMed Central; Volume: 1; Issue: 7 Linguagem: Inglês
10.1007/bf03401896
ISSN1528-3658
AutoresFabrizio Spinozzi, Elisabetta Agea, Onelia Bistoni, Nicola Forenza, Alessandro Monaco, Brunangelo Falini, Gabrio Bassotti, F. De Benedictis, Fausto Grignani, A Bertotto,
Tópico(s)Occupational exposure and asthma
ResumoT lymphocytes infiltrating airways during the allergic immune response play a fundamental role in recruiting other specialized cells, such as eosinophils, by secreting interleukin 5 (IL-5), and promoting local and systemic IgE synthesis by producing EL-4. Whether these presumed allergen-specific T cells are of mucosal or systemic origin is still a matter of conjecture. Immunophenotype, IL-4 production, and in vitro proliferative response to specific or unrelated allergens were analyzed in the bronchoalveolar lavage (BAL) fluid lymphocyte suspensions obtained from untreated patients with allergic asthma. Healthy subjects and patients affected by pulmonary sarcoidosis, a granulomatous lung disease characterized by infiltrating Th1 CD4+ lymphocytes, served as controls. The proportion of γδ T lymphocytes, mostly CD4+ or CD4−–CD8−, was higher in asthmatic subjects than in controls (p < 0.05). Most BAL γδ CD4+ lymphocytes of asthmatic patients displayed the T cell receptor (TCR)-γδ Vδ1 chain. While CD30 antigen coexpression on the surface of BAL αβ+ T lymphocytes was low (ranging from 5 to 12%), about half of pulmonary γδ T cells coexpressed it. These cells produced IL-4 and negligible amounts of interferon-γ (IFNγ), and proliferated in vitro in response to purified specific but not unrelated allergens. In contrast, control or sarcoidosis γδ T cells never displayed the CD30 surface molecule or produced significant quantities of EL-4. These findings not only confirm our previous hypothesis that the allergen-specific Th2-type lymphocytes found in the lungs of asthmatic patients are γδ T cells belonging to airway mucosal immunocytes, but also strongly support the notion that asthma is a local rather than a systemic disease.
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