RIE cytokines released from Th2 and Th2-like cells are likely to be ce
ntral to the pathophysiology of asthma and allergy, contributing to ab
errant IgE production, eosinophilia and, perhaps, mucosal susceptibili
ty to viral infection. IL-4 has emerged as a central tat get, not only
for B cell IgE production, but also in the commitment of both CD4+ an
d CD8+ T cells to cells with Th2 effector function capable of secretin
g IL-5 resulting in eosinophilic inflammation. In view of the central
role of this cytokine and the evidence that glucocorticoids are unable
to modify many IL-4 dependent effects, Th2 inhibitors may prove to be
novel therapies for the treatment of bronchial asthma.