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
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.