SUCCESSFUL TRANSFER OF LATE-PHASE EOSINOPHIL INFILTRATION IN THE LUNGBY INFUSION OF HELPER T-CELL CLONES

Citation
O. Kaminuma et al., SUCCESSFUL TRANSFER OF LATE-PHASE EOSINOPHIL INFILTRATION IN THE LUNGBY INFUSION OF HELPER T-CELL CLONES, American journal of respiratory cell and molecular biology, 16(4), 1997, pp. 448-454
Citations number
45
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
16
Issue
4
Year of publication
1997
Pages
448 - 454
Database
ISI
SICI code
1044-1549(1997)16:4<448:STOLEI>2.0.ZU;2-O
Abstract
Bronchial asthma is characterized by chronic eosinophilic inflammation of the bronchial mucosa. Accumulating evidences suggest that activate d T cells and T cell cytokines play critical roles in the local accumu lation and activation of eosinophils. To further delineate the critica l role of T cells on asthma, we tested the possibility whether eosinop hilic inflammation of the bronchial mucosa is induced by transferred T cell clones, in the absence of antigen-specific immunoglobulins (IgE, A, and G). Ovalbumin-specific Th2 clones were established and cytokin e profiles were determined. Eosinophilic inflammation accompanied with airway hyperresponsiveness occurred only when unprimed mice were tran sferred with IL-5 producing Th2 clones and challenged by the inhalatio n of relevant antigen. Increase of IL-5 concentration in bronchoalveol ar lavage fluid (BALF) was detected after the challenge, indicating th e local production of cytokines by the transferred T cells, and preced ed the appearance of the airway eosinophilia. Eosinophil infiltration was completely suppressed by the administration of anti-IL-5 neutraliz ing antibody, indicating the essential role of IL-5 in this model. The intensity of the eosinophil accumulation in vivo correlated well with the capacity of the T cell clones to produce IL-5 in vitro. We conclu ded that the existence of IL-5-producing helper T cells is sufficient for the development of the eosinophilic inflammation at the bronchial mucosa upon inhalation challenge of the relevant antigen.